China Military News & Updates

johnq

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COVID-19 was created in the Wuhan laboratory: Professor Giuseppe Tritto

Coronavirus which is killing and infecting people all over the world was created in a Lab in China's Wuhan, such an idea would have been labelled a conspiracy theory until a few weeks ago.

But earlier this week, a Chinese virologist Dr Li-Meng Yan, in an exclusive conversation with WION claimed that the deadly coronavirus was developed in a government laboratory in Wuhan. She also said that Chinese government was aware of the COVID-19 spread.

And now Professor Giuseppe Tritto, an internationally known expert in biotechnology and nanotechnology in his book 'China COVID 19: The chimera that changed the world' has said that he believes the Chinese Communist Party (CCP) is behind the Wuhan coronavirus (COVID-19), leaving little doubt that this viral “chimera” was artificially created as a bioweapon.

Earlier today — we spoke to professor Tritto, he says China has the capability to modify viruses — and develop bioweapons that — the Wuhan institute of virology — didn't follow the global standards for safety for a long time and — Chinese scientists were specifically working on bat coronaviruses — a project that was supervised by the military's top scientist She Zheng-lee.

Professor Tritto raises serious questions about the Wuhan lab it is called Asia’s largest virus bank scientists classify it as a "P-4" facility.

A lab that is supposed to follow the highest level of biosafety precautions, almost all major countries have a lab like this including India.

They follow global standards for safety and — these labs are open to inspection by the world but — not the Wuhan lab China does not follow global rules this facility has a checkered safety record professor Tritto told us — that the Wuhan lab only notified its safety measures last year. In 2019 it's been around since 2014 this lab was conducting studies on bat coronaviruses.

And interestingly, it is headed by china's leading expert on bioweapons-- the PLA's Major General Chen Wei what professor Tritto told us today— is what the world has long feared. He spoke to us from Rome.
Link for interview below:
Gravitas: Global biomedical expert: Virus could have leaked in Wuhan
 

johnq

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IS COVID-19 AN ‘UNRESTRICTED BIOWEAPON’?
Li-Meng Yan, A Chinese virologist (MD, PhD) who worked in a WHO reference lab and fled her position at the University of Hong Kong, has published a second co-authored report, alleging that SARS-CoV-2, the virus which causes COVID-19, was not only created in a Wuhan lab, it’s an “unrestricted bioweapon” which was intentionally released.
BY TYLER DURDEN FOR ZERO HEDGE


“We used biological evidence and in-depth analyses to show that SARS-CoV-2 must be a laboratory product, which was created by using a template virus (ZC45/ZXC21) owned by military research laboratories under the control of the Chinese Communist Party (CCP) government,” reads the paper.

SARS-CoV2 is a product of laboratory modification, which can be created in approximately six months using a template virus owned by a laboratory of the People’s Liberation Army (PLA). The fact that data fabrications were used to cover up the true origin of SARS-CoV 2 further implicates that the laboratory modification here is beyond simple gain-of-function research.
The scale and the coordinated nature of this scientific fraud signifies the degree of corruption in the fields of academic research and public health.
As a result of such corruption, damages have been made both tot he reputation of the scientific community and to the well-being of the global community.

The report also claims that the RaTG13 virus which Wuhan “Batwoman” Dr. Zhengli Shi and colleagues say they obtained in bat feces in 2013 (and which is 96% identical to SARS-CoV-2), is fraudulent and also man made.

Since its publication, the RaTG13 virus has served as the founding evidence for the theory that SARS-CoV-2 must have a natural origin. However, no live virus or an intact genome of RaTG13 have ever been isolated or recovered. Therefore, the only proof for the “existence” of RaTG13 in nature is its genomic sequence published on GenBank.

The report goes on to say that the RaTG13 genome could easily be fabricated, and that “an entry on GenBank, which in this case is equivalent to the existence of an assembled viral genomic sequence and its associated sequencing reads, is not a definitive proof that this viral genome is correct or real,” and that the process for sequencing DNA itself “leaves room for potential fraud.”

If one intends to fabricate an RNA viral genome on GenBank, he or she could do so by following these steps: create its genomic sequence on a computer, have segments of the genome synthesized based on the sequence, amplify each DNA segment through PCR, and then send the PCR products (may also be mixed with genetic material derived from the alleged host of the virus to mimic an authentic sequencing sample) for sequencing.The resulted raw sequencing reads would be used, together with the created genomic sequence, for establishing an entry on GenBank. Once accomplished, this entry would be accepted as the evidence for the natural existence of the corresponding virus. Clearly, a viral genomic sequence and its GenBank entry can be fabricated if well-planned.



RaTG13 has ‘multiple abnormal features,’ according to the report. For starters, it’s claimed that it was a fecal sample – yet just 1.7% of the raw sequencing reads are bacterial, when fecal swab samples are typically 70-90% bacterial. Second, the genomic sequence for RaTG13 contains segments of non-bat origin, including fox, flying fox, squirrels and other animals.

What’s more, China destroyed all evidence of RaTG13. “No independent verification of the RaTG13 sequence seems possible because, according to Dr. Zhengli Shi,the raw sample has been exhausted and no live virus was ever isolated or recovered. Notably, this information was known to a core circle of virologists early on and apparently accepted by them.”

Meanwhile, another coronavirus which shares a ‘100% nucleotide sequence identity with RaTG13’ – RaBtCoV/4991 – on a ‘short, 440-bp RNA-dependent RNA polymerase gene segment.’

RaBtCoV/4991 was allegedly discovered by Shi and colleagues in 2012 and published in 2016, and colleagues have been asking if it’s the same virus as RaTG13.

Given the 100% identity on this short gene segment between RaBtCoV/4991 and RaTG13,the field has demanded clarification of whether or not these two names refer to the same virus. However,Dr. Shi did not respond to the requestor address this question for months. The answer finally came from Peter Daszak, president of EcoHealth Alliance and long-term collaborator of Shi, who claimed that RaBtCoV/4991 was RaTG1327.

Three suspicious facts

First, it makes no sense that ‘Batwoman’ Shi and her team wouldn’t have conducted whole genome sequencing of RaBtCoV/4991 before 2020, as it was suspected in the deaths of miners who suffered from severe pneumonia after clearing out bat droppings in a Chinese mineshaft.

Given the Shi group’s consistent interests in studying SARS-like bat coronaviruses and the fact that RaBtCoV/4991 is a SARS-like coronavirus with a possible connection to the deaths of the miners, it is highly unlikely that the Shi group would be content with sequencing only a 440-bp segment of RdRpand not pursue the sequencing of the receptor-binding motif (RBM)-encoding region of the spike gene. In fact, sequencing of the spike gene is routinely attempted by the Shi group once the presence of a SARS-like bat coronavirus is confirmed by the sequencing of the 440-bp RdRpsegment25,32, although the success of such efforts is often hindered by the poor quality of the sample.

“Clearly, the perceivable motivation of the Shi group to study this RaBtCoV/4991 virus and the fact that no genome sequencing of it was done for a period of seven years (2013-2020) are hard to reconcile and explain.

Meanwhile, genomic sequencing of RaTG13 was conducted in 2018.

Second, why did Shi delay publication on RaTG13 until 2020 when it’s got a Spike protein that can bind with human ACE2 receptors?

…if the genomic sequence of RaTG13 had been available since 2018, it is unlikely that this virus, which has a possible connection to miners’ deaths in 2012 and has an alarming SARS-like RBM, would be shelfed for two years without publication. Consistent with this analysis, a recent study indeed proved that the RBD of RaTG13(produced via gene synthesis based on its published sequence) was capable of binding hACE2

Third, there has been no follow-up work on RaTG13 by Shi’s group.

Upon obtaining the genomic sequence of a SARS-like bat coronavirus, the Shi group routinely investigate whether or not the virus is capable of infecting human cells. This pattern of research activities has been shown repeatedly. However, such a pattern is not seen here despite that RaTG13 has an interesting RBM and is allegedly the closest match evolutionarily to SARS-CoV-2

Direct genetic evidence proving RaTG13 is fraudulent

Yan’s group closely examined the sequences of specific spike proteins for relevant viruses – specifically comparing mutations, and found that the spike genes of SARS-CoV-2 and RaTG13 do not contain evidence of natural evolution when compared to other coronaviruses which naturally evolved.

A logical interpretation of this observation is that SARS-CoV-2 and RaTG13 could not relate to each other through natural evolution and at least one must be artificial.If one is a product of natural evolution, then the other one must be not. It is also possible that neither of them exists naturally. If RaTG13 is a real virus that truly exists in nature, then SARS-CoV-2 must be artificial.

More:

It is highly likely that the sequence of the RaTG13 genome was fabricated by lightly modifying the SARS-CoV-2 sequence to achieve an overall 96.2% sequence identity. During this process, much editing must have been done for the RBM region of the S1/spike because the encoded RBM determines the interaction with ACE2 and therefore would be heavily scrutinized by others.

The paper concludes: All fabricated coronaviruses share a 100% amino acid sequence identity on the E protein with ZC45 and ZXC21

Evidence herein clearly indicates that the novel coronaviruses recently published by the CCP-controlled laboratories are all fraudulent and do not exist in nature. One final proof of this conclusion is the fact that all of these viruses share a 100% amino acid sequence identity on the E protein with bat coronaviruses ZC45 and ZXC21, which, as revealed in our earlier report1, should be the template/backbone used for the creation of SARS-CoV-2. Despite its conserved function in the viral replication cycle, the E protein is tolerant and permissive of amino acid mutations. It is therefore impossible for the amino acid sequence of the E protein to remain unchanged when the virus has allegedly crossed species barrier multiple times (between different bat species, from bats to pangolins, and from pangolins to humans). The 100% identity observed here, therefore, further proves that the sequences of these recently published novel coronaviruses have been fabricated.

Unrestricted bioweapon?

Yan notes that while it’s not easy for the public to accept that SARS-CoV-2 is a bioweapon due to its relatively low lethality, it indeed meets the criteria of a bioweapon.

In 2005, Dr. Yang specified the criteria for a pathogen to qualify as a bioweapon:
  1. It is significantly virulent and can cause large scale casualty.
  2. It is highly contagious and transmits easily, often through respiratory routes in the form of aerosols. The most dangerous scenario would be that it allows human-to-human transmission.
  3. It is relatively resistant to environmental changes, can sustain transportation, and is capable of supporting targeted release.
All of the above have been met bySARS-CoV-2: it has taken hundreds of thousands lives, led to numerous hospitalizations, and left many with sequela and various complications; it spreads easily by contact, droplets, and aerosols via respiratory routes and is capable of transmitting from human to human, the latter of which was initially covered up by the CCP government and the WHO and was first revealed by Dr. Li-Meng Yan on January 19th, 2020 on Lude Press; it is temperature-insensitive (unlike seasonal flu) and remains viable for a long period of time on many surfaces and at 4°C (e.g. the ice/water mixture).

What’s more, COVID-19 spreads asymptomatically, which “renders the control of SARS-CoV-2 extremely challenging.”

“In addition, the transmissibility, morbidity, and mortality of SARS-CoV-2 also resulted in panic in the global community, disruption of social orders, and decimation of the world’s economy. The range and destructive power of SARS-CoV-2 are both unprecedented.

“Clearly,SARS-CoV-2 not only meets but also surpasses the standards of a traditional bioweapon. Therefore, it should be defined as an Unrestricted Bioweapon.”
 
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johnq

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I am posting the newest article by Dr. Li-Meng Yan proving that Covid-19 virus is a bioweapon created in a Chinese military lab, and intentionally leaked out to the world. I am not including the referenced figures and citations (due to format limitations); the full report (in pdf format) with all figures and citations can be accessed via this link:
SARS-CoV-2 Is an Unrestricted Bioweapon: A Truth Revealed through Uncovering a Large-Scale, Organized Scientific Fraud
Li-Meng Yan (MD, PhD), Shu Kang (PhD), Jie Guan (PhD), Shanchang Hu (PhD)
Rule of Law Society & Rule of Law Foundation, New York, NY, USA.

Correspondence: [email protected]

Abstract

Two possibilities should be considered for the origin of SARS-CoV-2: natural evolution or laboratory creation. In our earlier report titled “Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route”, we disproved the possibility of SARS-CoV-2 arising naturally through evolution and instead proved that SARS-CoV-2 must have been a product of laboratory modification. Despite this and similar efforts, the laboratory creation theory continues to be downplayed or even diminished. This is fundamentally because the natural origin theory remains supported by several novel coronaviruses published after the start of the outbreak. These viruses (the RaTG13 bat coronavirus, a series of pangolin coronaviruses, and the RmYN02 bat coronavirus) reportedly share high sequence homology with SARSCoV- 2 and have altogether constructed a seemingly plausible pathway for the natural evolution of SARSCoV-2. Here, however, we use in-depth analyses of the available data and literature to prove that these novel animal coronaviruses do not exist in nature and their sequences have been fabricated. In addition, we also offer our insights on the hypothesis that SARS-CoV-2 may have originated naturally from a coronavirus that infected the Mojiang miners.

Revelation of these virus fabrications renders the natural origin theory unfounded. It also strengthens our earlier assertion that SARS-CoV-2 is a product of laboratory modification, which can be created in approximately six months using a template virus owned by a laboratory of the People’s Liberation Army (PLA). The fact that data fabrications were used to cover up the true origin of SARS-CoV-2 further implicates that the laboratory modification here is beyond simple gain-of-function research.

The scale and the coordinated nature of this scientific fraud signifies the degree of corruption in the fields of academic research and public health. As a result of such corruption, damages have been made both to the reputation of the scientific community and to the well-being of the global community.

Importantly, while SARS-CoV-2 meets the criteria of a bioweapon specified by the PLA, its impact is well beyond what is conceived for a typical bioweapon. In addition, records indicate that the unleashing of this weaponized pathogen should have been intentional rather than accidental. We therefore define SARS-CoV-2 as an Unrestricted Bioweapon and the current pandemic a result of Unrestricted Biowarfare.

We further suggest that investigations should be carried out on the suspected government and individuals and the responsible ones be held accountable for this brutal attack on the global community.

Introduction

SARS-CoV-2 is a novel coronavirus and the causative agent of the COVID-19 pandemic. Despite its tremendous impact, the origin of SARS-CoV-2, however, has been a topic of great controversy. In our first report titled “Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route”, we used biological evidence and in-depth analyses to show that SARS-CoV-2 must be a laboratory product, which was created by using a template virus (ZC45/ZXC21) owned by military research laboratories under the control of the Chinese Communist Party (CCP) government. In addition, resources and expertise are all in place in the Wuhan Institute of Virology (WIV) and related, other CCP-controlled institutions allowing the creation of SARS-CoV-2 in approximately six months.

What have not been fully described in our earlier analyses are details of the novel animal coronaviruses published by the CCP-controlled laboratories after the outbreak1. While no coronaviruses reported prior to 2020 share more than 90% sequence identity with SARS-CoV-2, these recently published, novel animal coronaviruses (the RaTG13 bat coronavirus, a series of pangolin coronaviruses, and the RmYN02 bat coronavirus9) all share over 90% sequence identities with SARS-CoV-2. As a result, these SARS-CoV-2-like viruses have filled an evolutionary gap and served as the founding evidence for the theory that SARS-CoV-2 has a natural origin. In this report, we provide genetic and other analyses, which, when combined with recent findings, prove that these novel animal coronaviruses do not exist in nature and their genomic sequences are results of fabrication.

1. Evidence proving that the RaTG13 virus is fraudulent and does not exist in nature

On February 3rd, 2020, Dr. Zhengli Shi and colleagues published an article in Nature titled “A pneumonia outbreak associated with a new coronavirus of probable bat origin” (manuscript submitted on January 20th), which was one of the first publications to identify SARS-CoV-2 as the pathogen causing the disease now widely known as COVID-19. Also reported in this article was a novel bat coronavirus named RaTG13, the genomic sequence of which was shown to be 96.2% identical to that of SARS-CoV-2. The close evolutionary relationship between RaTG13 and SARS-CoV-2 as suggested by the high sequence identity had led to a conclusion that SARS-CoV-2 has a natural origin. These striking findings have consequently made this article one of the most cited publications in the currently overwhelmed field of coronavirus research. Interestingly, an article published by Dr. Yong-Zhen Zhang and colleagues on the same issue of Nature, which also discovered SARS-CoV-2 as the responsible pathogen for COVID-19, received much less citations. This latter article made no mention of RaTG13. Instead, Zhang and colleagues showed that, evolutionarily, SARS-CoV-2 was closest to two bat coronaviruses, ZC45 and ZXC21, both of which were discovered and characterized by military research laboratories under the control of the CCP government. Immediately after the publication of this article, Dr. Zhang’s laboratory was shut down by the CCP government with no explanations offered.

Since its publication, the RaTG13 virus has served as the founding evidence for the theory that SARSCoV-2 must have a natural origin. However, no live virus or an intact genome of RaTG13 have ever been isolated or recovered. Therefore, the only proof for the “existence” of RaTG13 in nature is its genomic sequence published on GenBank.

1.1 The sequence of RaTG13 uploaded at GenBank can be fabricated

In order to have the sequence of a viral genome successfully uploaded onto GenBank, submitters have to provide both the assembled genomic sequence (text only) and raw sequencing reads. The latter is used for quality control and verification purposes. However, due to the huge amount of work involved in assembling raw reads into complete genomes, no sufficient curation is in place to ensure the correctness or truthfulness of the uploaded viral genomes. Therefore, an entry on GenBank, which in this case is equivalent to the existence of an assembled viral genomic sequence and its associated sequencing reads, is not a definitive proof that this viral genome is correct or real.

Sequencing of a viral RNA genome requires amplifying segments of it using reverse transcriptase PCR (RT-PCR) as the first step. The products of the RT-PCR, which are double-stranded DNA, would subsequently be sent for sequencing. The resulted sequencing reads, each ideally revealing the sequence of a segment of the genome, are then used to assemble the genome of the virus under study (Figure 1A).

Typically, some segments of the genome may not be covered by the initial round of sequencing. Therefore, gap filling will be carried out, where these missing segments will be amplified specifically and the DNA products subsequently sequenced. These steps are repeated until a complete genome can be assembled, ideally with a proper depth to ensure accuracy.

However, this process leaves room for potential fraud. If one intends to fabricate an RNA viral genome on GenBank, he or she could do so by following these steps: create its genomic sequence on a computer, have segments of the genome synthesized based on the sequence, amplify each DNA segment through PCR, and then send the PCR products (may also be mixed with genetic material derived from the alleged host of the virus to mimic an authentic sequencing sample) for sequencing (Figure 1B). The resulted raw sequencing reads would be used, together with the created genomic sequence, for establishing an entry on GenBank. Once accomplished, this entry would be accepted as the evidence for the natural existence of the corresponding virus. Clearly, a viral genomic sequence and its GenBank entry can be fabricated if well-planned.

The complete genomic sequence of RaTG13 was first submitted to GenBank on January 27th, 2020. The raw sequencing reads were made available on February 13th, 2020 (NCBI SRA: SRP249482).

However, the sequencing data for gap filling, which is indispensable in assembling a complete genome, was only made available on May 19th, 2020 (NCBI SRA: SRX8357956). The timing and the reversed order of events here are strange and suspicious.

The raw sequencing reads of RaTG13 have multiple abnormal features. Despite the sample being described as a fecal swab, only 0.7% of the raw sequencing reads are bacterial reads while the bacterial abundance is typically 70~90% when other fecal swab samples were sequenced. In addition, in the identifiable region of certain sequencing reads, a vast majority of reads are eukaryotic sequences, which is also highly unusual in the sequencing of fecal swap-derived samples. Within these eukaryotic reads, 30% of the sequences are of non-bat origin and instead shown to be from many different types of animals including fox, flying fox, squirrels, etc. These abnormal features are significant and indicate that the raw sequencing reads should have been obtained via a route that is different from the normal one (Figure 1).

No independent verification of the RaTG13 sequence seems possible because, according to Dr. Zhengli Shi, the raw sample has been exhausted and no live virus was ever isolated or recovered. Notably, this information was known to a core circle of virologists early on and apparently accepted by them. It was then made public, months later, by Dr. Yanyi Wang, director general of the WIV, in an TV interview on May 23rd, 2020. Dr. Shi also confirmed this publicly in her email interview with Science in July 2020.

However, judging from Shi’s published protocol, exhaustion of the fecal swap sample is highly unlikely. According to this protocol, the fecal swab sample would be mixed with 1 ml of viral transport medium and the supernatant collected. Every 140 ul of the supernatant would then yield 60 ul of extracted RNA. For the subsequent step, RT-PCR, 5 ul of this RNA-containing solution is required per reaction.

Therefore, from one fecal swab sample, at least 80 RT-PCR reactions could be carried out ([1000/140] x 60/5=86). Such an amount is sufficient to support both the initial round of sequencing and the subsequent gap filling PCR. It would be sufficient to also allow reasonable attempts to isolate live viruses, although Dr. Shi claimed that no virus isolation was attempted.

Therefore, the RaTG13 virus and its published sequence are suspicious and show signs of fabrication.

1.2 Other suspicions associated with RaTG13

RaTG13 was reported by Dr. Zhengli Shi from the WIV. Dr. Shi is a fellow of the American Academy of Microbiology and one of the most accomplished Chinese virologists. A peer-reviewed article authored by her and published on the top journal Nature, therefore, brought a great level of comfort for the coronavirus research community in accepting RaTG13 as a true, nature-born bat coronavirus. As a result, RaTG13, upon its timely publication, served as the founding evidence for the natural origin theory of SARS-CoV-2.

However, as revealed in section 1.1, the reported sequence of RaTG13, which is the only proof of the virus’ existence in nature, is problematic and shows signs of fabrication.
Intriguingly, despite the pivotal role of RaTG13 in revealing the origin of SARS-CoV-2, the
information provided for its discovery was surprisingly scarce with key points missing (location and date of sample collection, previous knowledge and publication of this virus, etc):

We then found that a short region of RNA-dependent RNA polymerase (RdRp) from a bat coronavirus (BatCoV RaTG13)—which was previously detected in Rhinolophus affinis from Yunnan province—showed high sequence identity to 2019-nCoV. We carried out full-length sequencing on this RNA sample (GISAID accession number EPI_ISL_402131). Simplot analysis showed that 2019-nCoV was highly similar throughout the genome to RaTG13 (Fig. 1c), with an overall genome sequence identity of 96.2%.

Only in the source section of the NCBI entry for RaTG13 (GenBank accession code: MN996532.1), one could find that the original sample was a “fecal swab” collected on “July 24th, 2013”. A closer look at the sequence reveals that RaTG13 shares a 100% nucleotide sequence identity with a bat coronavirus RaBtCoV/4991 on a short, 440-bp RNA-dependent RNA polymerase gene (RdRp) segment.

RaBtCoV/4991 was discovered by Shi and colleagues and published in 2016. As described in the 2016 publication, only a short 440-bp segment of RdRp of the RaBtCoV/4991 virus was sequenced then. Given the 100% identity on this short gene segment between RaBtCoV/4991 and RaTG13, the field has demanded clarification of whether or not these two names refer to the same virus. However, Dr. Shi did not respond to the request or address this question for months. The answer finally came from Peter Daszak, president of EcoHealth Alliance and long-term collaborator of Shi, who claimed that RaBtCoV/4991 was RaTG13.

RaBtCoV/4991 was discovered in the Yunnan province, China. In 2012, six miners suffered from severe pneumonia after clearing out bat droppings in a mineshaft in Mojiang, Yunnan, and three of them died soon afterwards. Although it was initially suspected that a SARS-like bat coronavirus may be responsible for the deaths, no coronavirus was either isolated or detected from the clinical samples. Also, first-hand record indicates failure of biopsy and no attempt of autopsy, which are the gold standards in the diagnosis of coronavirus infections. The pathogen responsible for the miners’ deaths therefore remained an unsolved case. (Detailed analyses of the Mojiang Miner Passage hypothesis, which was based on the miners’ case, are provided in section 1.6.) Despite the failed diagnosis, this unknown pathogen nonetheless triggered immense interests in the virologists in China. Three independent teams, including that of Dr. Shi’s, made a total of six visits to this mineshaft. The Shi group particularly looked for the presence of bat coronaviruses by amplifying and then sequencing a 440-bp RdRp segment, which is a routine procedure the Shi group follows in their surveillance studies. (As shown in section 2.1 of our first report, this RdRp segment is also frequently used for phylogenetic analyses and is an attractive target for antiviral drug discovery, which may have contributed to the design of incorporating a unique RdRp into the genome of SARS-CoV-2.) Out of the many coronaviruses detected, only RaBtCoV/4991 seemed to belong to the group of SARS-related, lineage B β coronaviruses.

The reporting of RaTG13 is suspicious in three aspects.

First, the whole genome sequencing of RaBtCoV/4991 should not have been delayed until 2020. Given the Shi group’s consistent interests in studying SARS-like bat coronaviruses and the fact that RaBtCoV/4991 is a SARS-like coronavirus with a possible connection to the deaths of the miners, it is highly unlikely that the Shi group would be content with sequencing only a 440-bp segment of RdRp and not pursue the sequencing of the receptor-binding motif (RBM)-encoding region of the spike gene. In fact, sequencing of the spike gene is routinely attempted by the Shi group once the presence of a SARS-like bat coronavirus is confirmed by the sequencing of the 440-bp RdRp segment, although the success of such efforts is often hindered by the poor quality of the sample.

As quoted above, in the 2020 Nature publication, Shi and colleagues strongly suggested that the sequencing of the full genome was done in 2020 after they discovered the resemblance between RaTG13 and SARS-CoV-2 on the short RdRp segment4. This, if true, suggests that the quality of the sample should not be poor. Therefore, there is no technical obstacle for the whole genome sequencing of RaBtCoV/4991.

Clearly, the perceivable motivation of the Shi group to study this RaBtCoV/4991 virus and the fact that no genome sequencing of it was done for a period of seven years (2013-2020) are hard to reconcile and explain.

However, an intriguing revelation took place in June 2020. Specifically, filenames of the raw sequencing reads for RaTG13 uploaded on the database were found, which indicate that these sequencing experiments were done in 2017 and 2018. Likely responding to this revelation, in her email interview with Science, Dr. Shi contradicted her own description in the Nature publication and admitted that the sequencing of the full genome of RaTG13 was done in 2018.

Second, RaTG13 has a remarkable RBM as suggested by its reported sequence, and the Shi group have no reason to delay its publication until 2020. The most critical segment of a SARS-like β coronavirus is the RBM in the Spike protein as it is fully responsible for binding the host ACE2 receptor and therefore determines the virus’ potential in infecting humans. The RBM is also the most variable region because it is under strong positive selection when the virus jumps over to a new host. Sequence alignment on this crucial RBM motif reveals that the RaTG13 virus rivals with the most highly regarded bat coronaviruses in terms of resemblance to SARS (Figure 2). RaTG13’s RBM not only is complete in reference to that of SARS but also is outstanding in its preservation of five residues perceived by Dr. Shi as key in binding human ACE2 (hACE2) (Figure 2, residues labeled with red texts). At position 472, RaTG13 is the only bat coronavirus that shares a leucine (L) residue with SARS, while the other four key residues are also largely conserved between the two viruses. Importantly, similar conservation patterns revealed in related bat coronaviruses, Rs3367 and SHC014, had led to their publication in Nature in 2013. Furthermore, viruses with less “attractive” RBM sequences (having large gaps and poor in the preservation of key residues, bottom half of the sequences in Figure 2) were also published by Dr. Shi in other top virology journals between 2013 and 2018. Therefore, if the genomic sequence of RaTG13 had been available since 2018, it is unlikely that this virus, which has a possible connection to miners’ deaths in 2012 and has an alarming SARS-like RBM, would be shelfed for two years without publication. Consistent with this analysis, a recent study indeed proved that the RBD of RaTG13 (produced via gene synthesis based on its published sequence) was capable of binding hACE2.

Third, no follow-up work on RaTG13 has been reported by the Shi group. Upon obtaining the genomic sequence of a SARS-like bat coronavirus, the Shi group routinely investigate whether or not the virus is capable of infecting human cells. This pattern of research activities has been shown repeatedly.

However, such a pattern is not seen here despite that RaTG13 has an interesting RBM and is allegedly the closest match evolutionarily to SARS-CoV-2.

Clearly, these three aspects deviate from normal research activities and logical thinking, which are difficult to reconcile or explain. They should have contributed to the intentional omission of key information in the reporting of RaTG13.

For publications of biological research, it is unethical for authors to change the name of a previously published virus without any notice or description. It is also unethical for authors to not cite their own

publication where they had characterized and reported the same virus. The violations here by Shi and colleagues on the reporting of RaTG13 are especially aggravating as the discovery of RaTG13 was central to uncovering the origin of SARS-CoV-2. By the time of the publication, SARS-CoV-2 had already led to many deaths in the city of Wuhan and had shown an alarming potential of causing a pandemic. In her much-delayed response to Science published on July 31st, 2020, Dr. Shi finally commented on the name change and stated that changing the name to RaTG13 was meant to better reflect the time and location of sample collection (TG = Tongguan; 13 = 2013). However, such an intention does not seem to justify why the previous name of RaBtCoV/4991 was never mentioned in the 2020 article and why they did not cite their own 2016 publication where RaBtCoV/4991 was first reported. Dr. Shi’s recent clarification did not alter the fact that they have violated the reporting norms of biological research.

In summary, a range of suspicions were associated with the reporting of RaTG13, including the violations of scientific publication principles, the inconsistency in the descriptions of the sequencing dates, and the contradiction between the sequencing of its genome in 2018 and the publication of it in 2020 when this virus has a striking RBM and a possible connection to pneumonia-associated deaths. Adding to these suspicions are the exquisite timing of its publication, the problematic nature of its reported sequence and raw sequencing reads, and the claim that no sample is left for independent verification. Collectively, these facts justify and legitimate the concern over the true existence of the RaTG13 virus in nature and the truthfulness of its reported genomic sequence. They also question the claim that the RaBtCoV/4991 virus and RaTG13 are equivalent.

1.3 Genetic evidence proving the fraudulent nature of RaTG13

This evidence was revealed after a close examination of the sequences of specific genes, especially spike, of relevant viruses. Specifically, we compared two viruses for the synonymous and nonsynonymous mutations on each gene, and we did so for two pairs of viruses. The first pair are bat coronaviruses ZC45 and ZXC21. The second pair are SARS-CoV-2 and RaTG13. The rationale for comparing these two pairs with each other is the following. First, ZC45 and ZXC21, each sharing an 89% genomic sequence identity with SARS-CoV-2, are the closest relatives to SARS-CoV-2 and RaTG13.

Second, ZC45 and ZXC21 are 97% identical to each other, while SARS-CoV-2 and RaTG13 are 96% identical. Not only the sequence identity in each case is comparable, but also the high sequence identity indicates that, within each pair, the sequence difference should be a result of random mutations during evolution, which ensures that synonymous and non-synonymous analyses here are appropriate and not complicated by abrupt evolutionary events (e.g. recombination). Indeed, sequence alignment confirms such a scenario – in both cases, the curve is smooth and the high sequence identity is maintained
throughout (Figure 3).

Detailed synonymous (syn, green curve) and non-synonymous (non-syn, red curve) analyses are shown in Figure 4. For each gene, the accumulations of syn and non-syn mutations, respectively, are illustrated when the codons are analyzed in a sequential order. For the spike genes, between ZC45 and ZXC21, the syn/non-syn ratio is 5.5:1 (Figure 4A left, 94 syn mutations and 17 non-syn mutations). Notably, the two curves progress along in a roughly synchronized manner. These features reflect, to a certain extent, the evolutionary traits resulted from random mutations during evolution in this sub-group of lineage B β coronaviruses.

The same analysis on the spike genes of SARS-CoV-2 and RaTG13, however, revealed a different scenario (Figure 4B right). Although the overall syn/non-syn ratio is a similar 5.4:1 (221 syn mutations and 41 non-syn mutations), the synchronization between the two curves is non-existent. In the second half of the sequence, which is over 700 codons (2,100 nucleotides) wide, the non-syn curve stays flat when the syn curve climbs continuously and significantly.

Counting the syn and non-syn mutations of the S2 region (corresponding to residues 684-1273 of the SARS-CoV-2 Spike) reveals that, between ZC45 and ZXC21, there are a total of 27 syn mutations and 5 non-syn mutations, yielding a syn/non-syn ratio of 5.4:1. In contrast, for the same S2 region, between SARS-CoV-2 and RaTG13, there are a total of 88 syn mutations and 2 non-syn mutations, yielding a syn/non-syn ratio of 44:1. The syn/non-syn ratios for S2, whole Spike, and other large viral proteins (Orf1a, Orf1b, and Nucleocapsid) are summarized in Table 1. While the ratios are comparable between the two groups for all other proteins, the ratios for the S2 protein are significantly different.

The detailed syn/non-syn analyses for Orf1a, Orf1b, and N are shown in Figure 4B-D. It is also noteworthy that, similar to that of Spike, the approximate synchronization between two curves is observed for the Orf1a protein in the ZC45 and ZXC21 comparison (Figure 4B left) but not in the SARS-CoV-2 and RaTG13 comparison (Figure 4B right).

The S2 protein maintains trimmer formation of the Spike and, upon successive cleavages to expose the fusion peptide, mediates membrane fusion and cell entry. Although the S2 protein is more conserved evolutionarily than S1, the extremely high purifying pressure on S2 as suggested by the very high syn/nonsyn ratio is abnormal. In fact, Orf1b is known to be the most conserved protein in coronaviruses and yet the syn/non-syn ratio for it is only 10.8:1 when SARS-CoV-2 and RaTG13 are compared, much lower than the ratio of 44:1 observed for S2 (Table 1). Furthermore, since RaTG13 and SARS-CoV-2 infect different species, no high purifying selection on S2 should be expected when these two viruses are compared against each other.

Consistent with the above notion, a syn/non-syn analysis done for the Spike protein of twenty randomly selected SARS-CoV-2 sequences showed that S2 was under positive selection, not purifying selection, during the past eight months of human-to-human transmission (Figure 5). For the twenty SARS-CoV-2 isolates, amino acid mutations are observed at five different locations in S2 (Figure 6). In addition, a recent study analyzing 2,954 genomes of SARS-CoV-2 revealed that mutations have been observed at 25 different locations in the S2 protein41, further proving that amino acid mutations are tolerated in S2 and no high purifying pressure should be observed for S2. Evidently, the syn/non-syn ratio of 44:1 revealed between SARS-CoV-2 and RaTG13 on the S2 region is abnormal (Table 1) and a violation of the principles of natural evolution.

A logical interpretation of this observation is that SARS-CoV-2 and RaTG13 could not relate to each other through natural evolution and at least one must be artificial. If one is a product of natural evolution, then the other one must be not. It is also possible that neither of them exists naturally.

If RaTG13 is a real virus that truly exists in nature, then SARS-CoV-2 must be artificial.

However, the reality is that SARS-CoV-2 is physically present and has first appeared prior to the reporting of RaTG13. This would then lead to the conclusion that RaTG13 is artificial, a scenario consistent with the overwhelming suspicion that this virus does not exist in nature and its sequence has been fabricated.

The remaining possibility is, of course, that both SARS-CoV-2 and RaTG13 are artificial: one has been created physically and the other one exists only in the form of a fabricated sequence.

It is highly likely that the sequence of the RaTG13 genome was fabricated by lightly modifying the SARS-CoV-2 sequence to achieve an overall 96.2% sequence identity. During this process, much editing must have been done for the RBM region of the S1/spike because the encoded RBM determines the interaction with ACE2 and therefore would be heavily scrutinized by others. An RBM too similar to that of SARS-CoV-2 would be troublesome because: 1) RaTG13 could be conceived as a product of gain-of-function research; 2) it would leave no room for an intermediate host and yet such a host is believed to exist as the Spike/RBM needs to first adapt in an environment where the ACE2 receptor is homologous to hACE2. In addition, modifying the sequence of the RBM is also beneficial as RaTG13 would otherwise appear to be able to infect humans as efficiently as SARS-CoV-2 does, escalating the concern of a laboratory leak. To eliminate such concerns, many non-syn mutations were introduced into the RBM region.

Importantly, syn/non-syn analysis is frequently used, often at the ORF/protein level, to characterize the

evolutionary history of a virus. While editing the RBM, the expert(s) carrying out this operation must be conscious of the need to maintain a reasonable syn/non-syn ratio for the whole Spike protein. To achieve so, however, the expert(s) must have then strictly limited the number of non-syn mutations in the S2 half of Spike, which ended up flattening the curve (Figure 4A right).

1.4 The receptor-binding domain (RBD) of RaTG13 does not bind ACE2 of horseshoe bats

Consistent with the above conclusion that RaTG13 does not exist in nature and its sequence was fabricated, a recent study showed that the RBD of RaTG13 could not bind the ACE2 receptors of two different kinds of horseshoe bats, Rhinolophus macrotis and Rhinolophus pusillus. Although the ACE2 receptor of Rhinolophus affinis (the alleged host of RaTG13) was not tested, it is unlikely that ACE2 of R. affinis would differ significantly from those of its close relatives and be able to bind the RaTG13 RBD.

This result therefore implicates that RaTG13 would not be able to infect horseshoe bats, contradicting the claim made by Shi and colleagues that the virus was detected and discovered from horseshoe bats. This is also consistent with the above conclusion that the genomic sequence of RaTG13 is fabricated and presumably computer-edited, which entails that the RBM/RBD suggested by the corresponding gene sequence may not be functional in binding the ACE2 receptor of the claimed host.

1.5 Conclusion and postulation of the fabrication process

In conclusion, the evidence presented both here and from recent literature collectively prove that RaTG13 does not exist in nature and its sequence has been fabricated.
If the RaBtCov/4991 virus is equivalent to RaTG13, then RaBtCoV/4991 must be fraudulent as well.

Apparently, in the actual process of sequence fabrication, the published sequence of the short RdRp segment of RaBtCoV/4991 was completely inherited for RaTG13. This way, they could claim that RaTG13 was RaBtCoV/4991, which, according to the record, was discovered in 2013. If RaTG13 had been described as being discovered right around the time of the COVID-19 outbreak, greater suspicions would result as tracing the evolutionary origin of a zoonotic virus is difficult and usually takes years or
decades. As described in section 2.1 of our earlier report1, the fabrication of RaTG13 should have been planned and executed in coordination with the laboratory creation of SARS-CoV-2.

Such an approach is also safe because, except for the 440-bp RdRp segment, no other sequence information has ever been published for the rest of the RaBtCoV/4991 genome.

It is worth noting that, due to reasons detailed in section 1.2, they still preferred to obscure the history of RaTG13. However, they must have also anticipated that their violations of the publication norms would invite inquiries or requests for clarifications, the number of which, however, should be limited and manageable. RaBtCoV/4991 would then function as an additional layer of security for them in facing such inquiries and/or requests.

Building upon the 440-bp RdRp sequence inherited from RaBtCoV/4991, the rest of the RaTG13 genome was likely fabricated by lightly editing the sequence of SARS-CoV-2. Once the genomic sequence was finalized, DNA fragments could be synthesized individually according to the fabricated and edited sequence and then used as templates for PCR. Amplified DNA would then be mixed with certain raw material to give the sample a natural look (mimicking what is present in an actual RT-PCR, which is done using RNA extracted from fecal swabs as templates). Subsequently, this sample would be sent for sequencing. The resulted raw sequencing reads could then be uploaded together with the made-up genomic sequence onto GenBank to create an entry for the RaTG13 genome.

1.6 The Mojiang Miner Passage (MMP) hypothesis is fatally flawed

Recently, a theory has emerged, which proposed that SARS-CoV-2 was derived from viral passaging in the lungs of the infected Mojiang miners back in 2012. Specifically, authors believe that the RaBtCoV/4991 virus was indeed RaTG13 and was the virus causing pneumonia in the miners in 2012.

While inside the lungs of the miners, the RaTG13 virus had evolved extensively, mimicking a viral passage process, and eventually became SARS-CoV-2. In this process, the RBD of the virus experienced strong positive selection, through which it became optimal in binding hACE2. Furthermore, the furin cleavage site at the S1/2 junction region of Spike had been acquired through recombination between the viral spike gene and the gene encoding the human ENaC protein, which has a furin-cleavage sequence closely resembling that of SARS-CoV-2. The end product of this passage was SARS-CoV-2, which the researchers isolated from the miners’ samples and brought back to the WIV. The authors have named this hypothesis as the Mojiang Miner Passage (MMP) hypothesis.

However, this MMP hypothesis has fatal flaws.

First, the viral pathogen that caused the disease in the miners could not be defined or confirmed.

According to the record, which was well documented in a Master’s Thesis written by the doctor in charge, samples from two patients (throat swabs and blood) were tested at the Center for Disease Control and Prevention of the Chengdu Military Region between May 15th and May 20th, 2012, and yet none of the suspected viruses, including SARS, was detected. Furthermore, the gold standard in the clinical diagnosis of coronavirus-caused pneumonia is biopsy and/or autopsy followed by confirmation by either RT-PCR or isolation of the virus. However, three biopsy tests were attempted but failed. Autopsy tests were requested and yet all turned down by families of the deceased miners. Due to such failure, both the Master’s Thesis and later a PhD Dissertation, which also looked into this issue although in an indirect manner, described the cause of the pneumonia as an unsolved case.

Second, antibody tests done for the miners do not support SARS or SARS-like coronavirus infection.

According to the Master’s Thesis, samples from two miners were tested for antibodies against SARS.

The symptoms onset date for one miner (case 3, passed away) was around April 13th, 2012. The other miner (case 4, had severe symptoms and yet recovered) had symptoms onset around April 16th, 2012.

Antibody tests, which were recommended later by Dr. Nanshan Zhong, were done at the WIV on June 19th, 2012. However, the two samples tested were only positive for IgM. No positive IgG or total antibody were reported. No antibody titer was reported either. Importantly, if the severe pneumonia was caused by coronavirus infections, by the time of the antibody tests on June 19th, 2012, both IgM and IgG/total antibody should be detected. In fact, IgG/total antibody should be much more abundant and easier to detect. On the other hand, IgM tests frequently result in false positives. Therefore, the fact
that only IgM, and no IgG/total antibody, was tested positive suggests that the described results were most likely false positives and the infections should not have been caused by SARS or a SARS-like coronavirus.

It is noteworthy that the later PhD Dissertation showed severe discrepancies with the Master’s Thesis in the descriptions of the same clinical tests:

1. The PhD Dissertation described that samples from four miners (throat swab and blood) were sent to the Center for Disease Control and Prevention of the Chengdu Military Region for nucleic acid tests. However, the Master’s Thesis indicated that samples were only taken from two miners.

2. The PhD Dissertation described samples from four miners were tested for anti-SARS antibodies at the WIV and all were IgG positive. However, the Master’s Thesis indicated that only samples from two miners were tested at the WIV and both were only IgM positive.

Importantly, the Master’s Thesis was written in 2013 in Yunnan by the doctor who was in charge of the six hospitalized miners. The PhD dissertation, however, was written in 2016 in Beijing based only on the clinical record. The author of the Dissertation had no direct involvement in the treatment of the miners or in any of the described tests. It is therefore highly likely that author of the PhD dissertation did not verify the clinical data he presented, which makes this PhD dissertation an unreliable source of information concerning the Mojiang miners’ case.

Third, if SARS-CoV-2 was already present in the miner’s body in 2012, it would have certainly caused an epidemic or even pandemic then. Given the extremely high transmissibility of SARS-CoV-2, it would be impossible for the doctors, nurses, family members of the miners, etc. to have avoided contracting the virus without the protection of proper PPE. If an epidemic indeed happened in 2012, it could not have gone unnoticed given the high transmissibility and lethality (three out of the six pneumonia patients died despite of intense medical care provided for them).

Fourth, as shown in sections 1.1-1.5, RaTG13’s sequence is clearly fabricated and the virus does not exist in nature. The RaBtCoV/4991 virus, which was detected in 2013, is not the RaTG13 virus that is defined by its reported genomic sequence. No complete genomic sequence of RaBtCoV/4991 has ever been reported likely due to the poor quality of the sample, which happens often as the RNA genome decays easily. It is highly likely that no high homology is shared between the actual RaBtCoV/4991 virus and SARS-CoV-2. This judgement is based on the fact that no viruses reported prior to 2020 share more than 90% sequence identity with SARS-CoV-2 despite the extensive surveillance studies of coronaviruses for the past two decades. Therefore, even if RaBtCoV/4991 was the pathogen responsible for the pneumonia of the miners, the theory that it has evolved in a single person’s lung into SARS-CoV-2 is far beyond being reasonable.

Fifth, it is impossible for the Spike protein of the virus to obtain a unique furin-cleavage site at the S1/S2 junction through recombination with the gene encoding the ENaC protein of the host cell (ENaC carries a furin cleavage site closely resembling the one seen in SARS-CoV-2). This is because recombination requires a significant level of sequence similarity between the two participating genes and yet no such similarity is present between coronavirus Spike and human ENaC. The molecular basis for recombination is non-existent. (Although recombination between ENaC and coronavirus Spike is impossible, it is suspicious that a viral protein and a host protein would share the same sequence for their furin-cleavage sites. It is possible, though, that the sequence of the furin-cleavage site in ENaC, which is known since 1997, could have been used in the design of the furin-cleavage site in the Spike of SARSCoV-2. Such a design may be considered sophisticated as ENaC co-expresses with ACE2 in many different types of cells.)

Sixth, if SARS-CoV-2 has indeed evolved from RaBtCoV/4991 in the miner’s lungs, it would look, from every aspect, like a naturally occurring virus. In that case, there would be no need to commit sequence fabrication for RaTG13 and for the other novel coronaviruses (parts 2 and 3) to falsify a natural origin for SARS-CoV-2.

Finally, as revealed in our earlier report, evidence exists in the genome of SARS-CoV-2, indicating that genetic manipulation is part of the history of SARS-CoV-2.

2. Evidence proving that recently published pangolin coronaviruses are fraudulent and do not exist in nature

While RaTG13 was reported to share a high sequence identity with SARS-CoV-2 and thereby hinted a natural origin of SARS-CoV-2, significant questions remained unanswered:

• No intermediate host has been found although one was believed to exist and function as the reservoir of the virus before it spilled over to humans.

• Despite the overall genomic resemblance of the two viruses, the RBD (particularly the RBM within it) of RaTG13 differs significantly from that of SARS-CoV-2. The evolutionary origin of the SARS-CoV-2 RBD, which is optimal in binding hACE2, remained unclear.

• A critical furin-cleavage site, which is present at the S1/S2 junction of SARS-CoV-2 Spike and responsible for the enhanced viral infectivity and pathogenicity, is absent in RaTG13 (as well as in all known lineage B β coronaviruses). The evolutionary origin of this furin-cleavage site also remained mysterious.

Not long after these questions emerged, several laboratories published novel coronaviruses allegedly found in Malayan pangolins that were smuggled from Malaysia and confiscated by the Chinese custom. Although these novel coronaviruses share relatively lower overall sequence identities (~90%) with SARS-CoV-2 in comparison to RaTG13 (96.2% identical to SARS-CoV-2), the RBD of the pangolin coronaviruses resembles greatly the SARS-CoV-2 RBD (97.4% identical). In the most critical RBM
region, all amino acids except one are identical between the pangolin coronaviruses and SARS-CoV-2.

These observations led the authors to conclude 1) that pangolins are the likely intermediate host for the zoonotic transfer of SARS-CoV-2 and 2) that a RaTG13-like ancestor coronavirus might have acquired the RBD from a pangolin coronavirus through recombination to eventually become SARS-CoV-2.

Here, in part 2 of the report, we describe literature evidence and provide genetic analyses to prove that these novel pangolin coronaviruses are results of fabrication.

2.1 A single batch of pangolin samples were used in all studies and the deposited sequencing data showed heavy contamination and signs of fabrication

In October 2019, a team formed by three researchers from two institutions (Guangdong Institute of Applied Biological Resources and Guangzhou Zoo) reported, for the first time, the detection of coronavirus infections in pangolins that were allegedly smuggled from Malaysia and confiscated in the Guangdong province in March 2019. Twenty-one pangolin samples were sequenced and five were positive for coronavirus infections (Table 2: lung 2, 7, 8, 9, and 11), although Sendai virus infection was also reported. However, neither the sequences of the coronaviruses nor raw sequencing data were made available to the public for a period of three months. The raw data (NCBI BioProject PRJNA573298) was finally released on January 22nd, 2020 after the COVID-19 outbreak started, while the article submission date was September 30th, 2019 and the publication date was October 24th, 2019.

Between March and May 2020, four seemingly independent studies were published, all of which reported novel pangolin coronaviruses and their assembled genomic sequences. However, after a closer look, we found that all four studies derived viral sequences from the same set of pangolin samples first reported in the October 2019 publication, which has been confirmed by a recent article.

In one study, Liu et al. (the same authors of the October 2019 publication) re-assembled the genome of a pangolin coronavirus by pooling two samples from the original 2019 study and one sample obtained from another Malayan pangolin rescued in July 2019. However, although the authors stated that the more recent raw sequencing data had been deposited at the NCBI database, we could not find this data using the accession number (2312773) provided. The same difficulty has been reported by others. Therefore, it cannot be verified whether the July 2019 dataset truly exists and has contributed to the assembly of the reported genome.

In two other studies, Lam et al. and Zhang et al. each re-assembled the genome of a pangolin coronavirus using only the published dataset from the October 2019 study. Lam et al. also reported detection of coronaviruses from smuggled Malayan pangolins that were confiscated in the Guangxi province, although these viruses showed lower sequence identities to SARS-CoV-2 both at the whole genome level (~86%) and in the critical RBD region. It is noteworthy that this study was done as a collaboration between Dr. Yi Guan’s group from the University of Hong Kong and Dr. Wuchun Cao’s group from the Academy of Military Medical Sciences (AMMS), Beijing, China. Somehow, all authors affiliated with the AMMS were excluded from the list of authors when the article was first submitted, although their names eventually appeared in the final version of the publication.

In the fourth study, Xiao et al. claimed to have examined tissue samples kept from diseased pangolins and obtained raw sequencing data for the subsequent assembly. However, they did not describe how the samples were acquired. In their Extended Data Table 3, they listed the metagenome sequencing data used in the study, which, surprisingly, do not match with the actual data that they uploaded in the database (Table 2). Samples M1, M5, M6, M10, and Z1 can be found in the data they deposited, but not M2, M3, M4, and M8. Furthermore, Xiao et al. apparently were inconsistent with the reporting of these raw sequencing reads. For samples M1, M6, pangolin3, and pangolin5, they counted paired ends numbers, which reflect the actual number of sequenced DNA fragments in the library. For the rest of samples, the authors counted reads numbers instead (In Illumina sequencing, there are two reads per fragment). For samples M2, M3, M4, and M8 in this latter group, when the reads numbers were converted to paired ends numbers (divided by 2), they each match perfectly with lung07, lung02, lung08, and lung11, respectively, from the October 2019 study (Table 2). Clearly, Xiao et al. used the data published in a previous study but failed to disclose this necessary information in their publication. In fact, they intentionally presented the “number of reads” in a different format to presumably make readers overlook the fact that the same sequencing dataset was used.

It is noteworthy that the study by Xiao et al. was also done in collaboration with the AMMS. Prior to the publication of the manuscript, this work was first publicized in a press conference. As revealed in this conference, four principle investigators contributed to the work and one of them was Dr. Ruifu Yang from the AMMS. However, like what happened to Dr. Cao and his AMMS colleagues in the Lam et al. study, Dr. Yang’s name was excluded in the submitted manuscript of Xiao et al. Yet, unlike the other case, the AMMS researcher’s name did not re-appear in the final publication. It is also noteworthy that the two AMMS principle investigators here, Dr. Yang and Dr. Cao, are long-term collaborators and most of their collaborative work concerned genetic analyses of SARS-CoV.

Among the four studies, only two assembled complete genomes by performing gap filling using PCR.

However, neither group made their gap filling sequences available, rendering independent verification impossible. Notably, the delayed publishing of raw sequencing reads long after the publication of genomic sequences has occurred in the reporting of RaTG13 as well.

Adding to the above problems was the poor quality of the raw sequencing data, which has been described recently. We also analyzed the composition of the sequencing reads of the deposited libraries. By performing taxonomy analysis on the NCBI SRA database, we also found that samples from Liu et al. that are positive for coronavirus reads are all positive for reads that map to human genome (Table 2). In great contrast, the rest of the samples, which are negative for viral reads, also have no human reads detected. The same correlation is found in data presented by Xiao et al. Although samples M5 (pangolin 6) and M6 (pangolin2) are negative for human reads, these two samples have very few viral reads, which would hardly contribute to the viral genome assembly. Clearly, the human contamination should not be due to sample handling as none of the coronavirus-negative samples, which must have been handled similarly, contain such contamination. The consistent co-existence of viral reads and human reads are highly suspicious.

These observations raise red flags not only on the credibility of the assembled sequences but also on the authenticity of these novel pangolin coronaviruses. It is also noteworthy that the manuscript submission dates for all four studies were between February 7th and February 18th, suggesting that their publications might have been coordinated.

2.2 No coronavirus was detected in an extensive surveillance study of Malayan pangolins

While these SARS-CoV-2-like pangolin coronaviruses were described as being detected in smuggled Malayan pangolins, a recent study strongly refuted the presence of such pangolin coronaviruses in nature.

A team led by Dr. Daszak examined 334 pangolin samples, which were collected in Malaysia and Sabah from August 2009 to March 2019. Surprisingly, no coronaviridae, or any of the other families of viruses (filoviridae, flaviviridae, orthomyxoviridae, and paramyxoviridae), were detected in any of these samples.

This is in stark contrast with the October 2019 publication where both coronavirus infection and Sendai virus infection were reportedly detected in the smuggled Malayan pangolins, which eventually led to the discovery and publication of the novel pangolin coronaviruses. The finding of Lee et al. adds significantly to the existing suspicions and substantiates the possibility that these pangolin coronaviruses do not exist in nature and their sequences could have been fabricated.

2.3 The RBD of the reported pangolin coronaviruses binds poorly to pangolin ACE2

If pangolin coronaviruses truly exist and have recently spilled over to infect humans, their Spike protein, especially the RBD within Spike, should bind to pangolin ACE2 (pACE2) more efficiently than to hACE2.

However, recent findings have contradicted this theory. In an in silico study, Piplani et al. calculated, following homology structural modeling, the binding energies involved in the association between SARSCoV-2 Spike and ACE2 from either human or various animals. Interestingly, the most favorable interaction that SARS-CoV-2 Spike makes was shown to be with hACE2, but not with ACE2 from pangolin or any other suspected intermediate host. Furthermore, another study revealed, using a robust in vitro binding assay, that the RBD of SARS-CoV-2 binds much tighter (greater than 9-fold) to hACE2 than to pACE2. Although the RBD of the pangolin coronaviruses is not 100% identical to that of SARSCoV-2, the RBMs of the two viruses, which is the most essential segment responsible for ACE2 interactions, differ only by one amino acid. Therefore, the poor binding efficiency observed between the RBD of SARS-CoV-2 and pACE2 infers that the RBD of the reported pangolin coronaviruses must bind to pACE2 fairly inefficiently. Indeed, a very recent study confirmed the case: the RBD of the pangolin coronavirus binds pACE2 ten-fold weaker than to hACE2. These observations once again refute the claim that pangolins are the probable intermediate host for SARS-CoV-2. More importantly, the latter two studies strongly suggest that these viruses might not be able to establish infections in pangolins, which adds significantly to the suspicion that the published sequences of the pangolin coronaviruses may have been fabricated and these viruses do not exist in nature.

2.4 Genetic evidence proving the fraudulent nature of the pangolin coronaviruses

Evolutionarily, within the coronavirus genome, the RBD of Spike is under the strongest positive selection as it needs to adapt for binding a new receptor whenever the virus crosses the species barrier and enters a new host. In lineage B β coronaviruses, the most essential segment for receptor recognition is the RBM, which fully determines the binding with ACE2. Strikingly, when the RBM sequence of the pangolin virus MP789 is compared to that of SARS-CoV-2, no positive selection is observed (Figure 7A). Instead, the analysis revealed very strong purifying selection with 24 syn mutations and only one non-syn mutation.

In contrast, when two related bat coronaviruses, BM48-31 and BtKY72, are compared in a similar manner, strong positive selection is observed as expected (Figure 7B). Here, while there are 25 syn mutations, which is comparable to that between MP789 and SARS-CoV-2, the number of non-syn mutations is 30 (Figure 7B). Evidently, the species difference between pangolin and human is greater than that between the hosts of BM48-31 and BtKY72, which are two different species of bats. Therefore, greater positive selection should be expected between MP789 and SARS-CoV-2 than that between BM48-31 and BtKY72. The strong purifying selection observed between MP789 and SARS-CoV-2 is, therefore, contradictory to the principles of natural evolution.

We further looked at the syn and non-syn mutations for the RBM in coronaviruses infecting the same species. Here, we compared the closely related coronaviruses ZC45 and ZXC21, which infect the same species of bats, on their RBM segments (Figure 7C). Here, twelve synonymous mutations and three nonsynonymous mutations are observed, yielding a syn/non-syn ratio of 4:1. Such a value likely represents the approximate upper limit for the purifying selection in the RBM that such coronaviruses could possibly experience (Table 3). In addition, no purifying selection is observed in the RBM for the randomly selected twenty SARS-CoV-2 sequences (Figure 5, codon range 437-507).

Therefore, the extremely high syn/non-syn ratio (24:1) observed between MP789 RBM and
SARSCoV-2 RBM indicates that at least one of the two viruses is artificial.

We believe that, to falsify the natural existence of the unique RBD/RBM of SARS-CoV-2, the amino acid sequence of the pangolin coronavirus RBD/RBM had been fabricated to closely resemble that of SARS-CoV-2. At the same time, the expert(s) carrying out this operation also wanted to create an appropriate level of divergence between the pangolin virus and SARS-CoV-2 at the nucleotide level and thereby introduced a significant amount of syn mutations in the RBM. The abnormality revealed in Figure 7A and Table 3 likely resulted from these fraudulent operations.

Similar syn/non-syn analyses on the overall spike further revealed the fraudulent nature of these novel pangolin coronaviruses. Here we compared two representative pangolin coronaviruses MP789 (a Guangdong isolate) and P4L (a Guangxi isolate) as genomic sequences within each group of isolates share very high sequence identities. As shown in Figure 8A, similar to the abnormal pattern observed between RaTG13 and SARS-CoV-2 (Figure 4A right), syn and non-syn curves exhibit drastically different trajectories and the non-syn curve abruptly flattens in the S2 half of the sequence.

For comparison, we also analyzed the spike genes of two SARS-like bat coronaviruses, BM48-31 and BtKY72. The two pangolin coronaviruses, MP789 and P4L, are 85.2% identical on the overall genome, while bat coronaviruses BM48-31 and BtKY72 are 82.4% identical. The comparison here is therefore appropriate. Analysis of the two bat viruses show that the two curves grow naturally in a relatively concerted manner with no excessive flattening of the red curve observed (Figure 8B).

Counting the number of syn and non-syn mutations in each pair of comparisons further illustrated the unnatural characteristics associated with the pangolin coronaviruses (Table 4). While the S2 protein is not expected to be more conserved than Orf1b, the syn/non-syn ratio for S2 observed in the comparison between MP789 and P4L is abnormally high (207 syn mutations and 9 non-syn mutations; syn/non-syn = 23:1), which is far exceeding what is observed for Orf1b (7.6:1).

As the two bat coronaviruses here were discovered in nature independently by research groups outside of China, the features displayed in Figure 8B likely represent the approximate evolutionary trait of two coronaviruses at this level of overall divergence. According to the logic described earlier, the great contrast between Figure 8A and 8B and the abnormal syn/non-syn ratio of 23:1 (Table 4) further prove that, between MP789 and P4L, at least one is artificial, although we believe both groups of pangolin coronaviruses represented by MP789 and P4L, respectively, are non-natural and fabricated.

2.5. Summary and discussion

A single source of samples was used for all studies (some spuriously independent7) reporting novel pangolin coronaviruses. The formats of sequencing reads were manipulated with a clear intention to hide the fact that the same dataset was used in different studies. The raw sequencing data is missing for certain critical pieces, poor in quality, and suspicious in terms of the amounts and types of contaminations present.

The RBD encoded by the reported sequence of pangolin coronaviruses could not bind pACE2 efficiently.

As revealed by syn/non-syn analyses, sequences of the RBM and S2 regions of these pangolin coronaviruses exhibit features that are inconsistent with natural evolution. Finally, no coronavirus was detected in a large, decade-long surveillance study of Malayan pangolins. These observations and evidence converge to prove that these recently reported pangolin coronaviruses do not exist in nature and their sequences must have been fabricated.

It is noteworthy that the abnormal syn/non-syn feature revealed for S2 in the comparison between MB789 and P4L (Figure 8A) resembles greatly that exhibited by the comparison between RaTG13 and SARS-CoV-2 (Figure 4A right). Judging based on this reoccurring pattern, we believe that the sequence fabrications in both cases (RaTG13 and pangolin coronaviruses) were most likely carried out by the same person or group, whose misconception of the spike gene evolution persisted in multiple such practices and resulted in the unnatural look of the syn/non-syn curves and numbers (Figure 4, Table 1, Figure 8, and Table 4).

3. Evidence revealing the fraudulent nature of the novel bat coronavirus RmYN02

While the publications of the fabricated pangolin coronaviruses might have seemingly fulfilled the scientific quests for an intermediate host for the zoonosis of SARS-CoV-2 as well as for an evolutionary origin of its RBD, it had remained suspicious and unexplainable how SARS-CoV-2 could have acquired the furin-cleavage site (-PRRAR/VS-) at the S1/2 junction through natural evolution. It is evident that, although furin-cleavage site has been found in certain other lineages of coronaviruses at the S1/2 junction, lineage B β coronaviruses clearly lack the ability to develop this motif at this location naturally.

In early June, another novel bat coronavirus, RmYN02, was reported9, which shares a 93.3% sequence identity with SARS-CoV-2 and appears to be the second closest bat coronavirus to SARS-CoV-2 (the closest is allegedly RaTG13). This finding adds yet another member to the rapidly growing sub-lineage of SARS-CoV-2-like coronaviruses (Figure 9), which has been completely vacant and practically nonexistent prior to the current pandemic. In addition, importantly, RmYN02 carries a unique sequence -PAA at the S1/S2 junction, which remotely resembles the inserted -PRRA- sequence at the same location in the SARS-CoV-2 Spike. Despite the fact that -PAA- in RmYN02 only partially resembles the -PRRA insertion in SARS-CoV-2 and does not appear to be an actual insertion if properly aligned, the authors nonetheless claimed that the natural occurrence of -PAA- in RmYN02 proves that the -PRRA- sequence could very likely be acquired and “inserted” into the same location in SARS-CoV-2 genome through natural evolution.

The fact that a poor alignment was used to make a disproportional, strong argument for an evolutionary origin of the furin-cleavage site, which appeared to be the last missing piece of the puzzle, is suspicious.

Furthermore, despite the significance of the spike sequence of RmYN02 in supporting the central conclusion of the publication, the raw sequencing reads for spike has not been made available although the authors stated otherwise in the article. This is yet another repeat of the pattern that has been exhibited in the reporting of both RaTG13 and pangolin coronaviruses, where the genomic sequence would be published first and the raw sequencing reads would not be made available months afterwards.

Given that the CCP-controlled laboratories have repeatedly engaged in fabrication of coronaviruses to feed the missing pieces for the puzzle, the above suspicion opens up the possibility that the RmYN02 virus could have been fabricated as well. Judging from the fact that its sequence identity to SARS-CoV-2 (93.3%) is lower than that between RaTG13 and SARS-CoV-2 (96.2%), we suspected that the sequence of RmYN02 might have been fabricated by modifying the sequence of RaTG13. Such an approach could easily ensure that the evolutionary distance between RmYN02 and SARS-CoV-2 is greater than that between RaTG13 and SARS-CoV-2. It also ensures that RmYN02 and RaTG13 would appear to be evolutionarily close, consistent with the claim that they both infect bats although of different species.

We therefore compared the spike genes of RmYN02 and RaTG13 on the quantity and distribution of syn and non-syn mutations. The severe divergence at the S1 portion between the two viral sequences did not allow the S1 sequences to be properly codon-aligned. Therefore, only the S2 half was analyzed (Figure 10). For the beginning 200 codons of S2, both types of mutations accumulate steadily and gradually.

However, for the final 378 codons, once again, the non-syn curve flattens and the concerted growth of the two curves has disappeared. In this region, there are 57 syn mutations and only one non-syn mutation. The syn/non-syn ratio of 57:1 for a region as wide as 378 codons (1,344 nucleotides) is severely inconsistent with what is observed naturally (Figure 4A left and Figure 8B).

Logically, between RaTG13 and RmYN02, at least one must be artificial. Here, however, we are convinced that both viruses are artificial. As shown in part 1, the sequence of RaTG13 must have been fabricated. Therefore, the fact that the last 378 codons of RmYN02’s S2 are identical, with the exception of one, to that of RaTG13 proves that the RmYN02 sequence must be artificial as well. This also proves our earlier suspicion that the RaTG13 sequence should have been used as the template for the fabrication of the RmYN02 sequence. RaTG13 was published in late January, while RmYN02 was published in early June (manuscript submitted in April). Therefore, enough time is in between for the sequence fabrication to be carried out.

While introducing nucleotide changes to create the apparent divergence between the two viruses, the expert(s) may have overly restricted amino acid changes in this part of Spike. Again, the abrupt change of trajectory of the non-syn curve and its excessive flattening later in the sequence likely reflect their overestimation of the purifying selection pressure on S2. The fact that this abnormal pattern has been observed in all three cases (Figure 4A right, 8A, and 10) reiterates the point raised in section 2.5 that all sequence fabrications may have been carried out by the same person or group.

4. Final discussion and remarks

4.1 All fabricated coronaviruses share a 100% amino acid sequence identity on the E protein with ZC45 and ZXC21


Evidence herein clearly indicates that the novel coronaviruses recently published by the CCP controlled laboratories are all fraudulent and do not exist in nature. One final proof of this conclusion is the fact that all of these viruses share a 100% amino acid sequence identity on the E protein with bat coronaviruses ZC45 and ZXC21, which, as revealed in our earlier report1, should be the template/backbone used for the creation of SARS-CoV-2 (Figure 11). Despite its conserved function in the viral replication cycle, the E protein is tolerant and permissive of amino acid mutations. It is therefore impossible for the amino acid sequence of the E protein to remain unchanged when the virus has allegedly crossed species barrier multiple times (between different bat species, from bats to pangolins, and from pangolins to humans). The 100% identity observed here, therefore, further proves that the sequences of these recently published novel coronaviruses have been fabricated.

A main goal of these fabrications was to obscure the connection between SARS-CoV-2 and ZC45/ZXC21. Therefore, from their perspective, the fabricated viruses should resemble SARS-CoV-2 more than ZC45 and ZXC21 do. Because ZC45 and ZXC21 already share a 100% identity with SARSCoV-2 on the E protein, the fabricated viruses therefore were made to adopt this sequence completely as well.

4.2 Important implications of this large-scale, organized scientific fraud

If SARS-CoV-2 is of a natural origin, no fabrications would be needed to suggest so. The current report, therefore, corroborates our earlier report and further proves that SARS-CoV-2 is a laboratory product.

As revealed, the creation of SARS-CoV-2 is convenient by following established concepts and techniques, some of which (for example, restriction enzyme digestion) are considered classic and yet still preferred widely including by experts of the field. A key component of the creation, the template virus ZC45/ZXC21, is owned by military research laboratories.

Importantly, as revealed here, multiple research laboratories and institutions have engaged in the fabrication and cover-up. It is clear that this was an operation orchestrated by the CCP government.

In addition, raw sequencing reads for RaTG13, which were integral parts of the fabrication, were obtained in 2017 and 2018. Furthermore, manuscript reporting the falsified coronavirus infections of Malayan pangolins was submitted for publication in September 2019. Evidently, the cover-up had been planned and initiated before the COVID-19 outbreak. Therefore, the unleashing of the virus must be a planned execution rather than an accident.

4.3 SARS-CoV-2 is an Unrestricted Bioweapon

Although it is not easy for the public to accept SARS-CoV-2 as a bioweapon due to its relatively low lethality, this virus indeed meets the criteria of a bioweapon as described by Dr. Ruifu Yang. Aside from his appointment in the AMMS, Dr. Yang is also a key member of China’s National and Military Bioterrorism Response Consultant Group and had participated in the investigation of the Iraqi bioweapon program as a member of the United Nations Special Commission (UNSCOM) in 1998. In 2005, Dr. Yang specified the criteria for a pathogen to qualify as a bioweapon:

1. It is significantly virulent and can cause large scale casualty.

2. It is highly contagious and transmits easily, often through respiratory routes in the form of aerosols.
The most dangerous scenario would be that it allows human-to-human transmission.

3. It is relatively resistant to environmental changes, can sustain transportation, and is capable of supporting targeted release.

All of the above have been met by SARS-CoV-2: it has taken hundreds of thousands lives, led to numerous hospitalizations, and left many with sequela and various complications; it spreads easily by contact, droplets, and aerosols via respiratory routes and is capable of transmitting from human to human, the latter of which was initially covered up by the CCP government and the WHO and was first revealed by Dr. Li-Meng Yan on January 19th, 2020 on Lude Press; it is temperature-insensitive (unlike seasonal flu) and remains viable for a long period of time on many surfaces and at 4°C (e.g. the ice/water mixture).

Adding to the above properties is its high rate of asymptomatic transmission, which renders the control of SARS-CoV-2 extremely challenging. In addition, the transmissibility, morbidity, and mortality of SARS-CoV-2 also resulted in panic in the global community, disruption of social orders, and decimation of the world’s economy. The range and destructive power of SARS-CoV-2 are both unprecedented.

Clearly, SARS-CoV-2 not only meets but also surpasses the standards of a traditional bioweapon.

Therefore, it should be defined as an Unrestricted Bioweapon.

4.4 The current pandemic is an attack on humanity

The scientific evidence and records indicate that the current pandemic is not a result of accidental release of a gain-of-function product but a planned attack using an Unrestricted Bioweapon. The current pandemic therefore should be correspondingly considered as a result of Unrestricted Biowarfare.

Under such circumstances, the infected population are being used, unconsciously, as the vectors of the disease to facilitate the spread of the infection. The first victims of the attack were the Chinese people, especially those in the city of Wuhan. At the initial stage, the hidden spread in Wuhan could have also served another purpose: the final verification of the bioweapon’s functionality, an important aspect of which is the human-to-human transmission efficiency. Upon the success of this last step, targeted release of the pathogen might have been enabled.

Given the global presence of SARS-CoV-2 and the likelihood of its long-term persistence, it is appropriate to say that this attack was on the humanity as a whole and has put its fate at risk.

4.5 Actions need to be taken to combat the current pandemic and save the future of humanity

Given the CCP’s role here, it is of paramount importance that the CCP is held accountable for its actions.

In addition, the world needs to find out what other variants of SARS-CoV-2 exist in the CCP-controlled laboratories, whether or not SARS-CoV-2 or its variant(s) are still being actively released, whether or not re-infection of SARS-CoV-2 leads to worsened outcomes due to inefficient immunity and/or antibody dependent enhancement (ADE), and whether other weaponized pathogens are owned by the CCP as a result of their excessive, state-stimulated efforts in collecting novel animal pathogens and studying their potentials in zoonosis.

It is also of paramount importance that all the hidden knowledge of SARS-CoV-2 be brought out as soon as possible. As illustrated in our earlier report, although a template virus was used, the creation of SARS-CoV-2 must have involved introducing changes to the template sequence through DNA synthesis (steps 1 and 4 in part 2 of our earlier report)1. Such a practice can be safely guided by multi-sequence alignment of available SARS and SARS-like coronavirus sequences. The process of this practice has been illustrated, and both syn mutations and amino acid (non-syn) mutations at variable positions/regions would be introduced. From the perspective of the responsible scientists, these changes are necessary because, otherwise, the engineered nature of the virus and its connection to its template would be evident.

However, importantly, the introduced changes might have also altered the functions of the various viral components, which could be either by design or unintended. Nonetheless, it remains to be answered whether or how the introduced changes might be responsible for the various lasting complications that many COVID-19 patients experience and what barriers these changes might pose to the development of effective vaccines and other antiviral therapeutics. It is reasonable to believe that the responsible laboratories under the control of the CCP have been engaged in this research for a long period of time and therefore keep in possession a considerable amount of concealed knowledge of SARS-CoV-2. Some of the knowledge may provide answers to questions that need to be addressed urgently in the global combat against COVID-19. Such hidden knowledge ought to be made available to the world immediately.

What also need to be held accountable are the individuals and groups within certain organizations and institutions in the fields of public health and academic research, who knowingly and collaboratively facilitated the CCP’s misinformation campaign and misled the world. On January 18th and 19th, 2020, Dr. Li-Meng Yan, then anonymously, first revealed that SARS-CoV-2 is of a laboratory origin.

Immediately afterwards, on January 20th, Dr. Zhengli Shi submitted her manuscript to Nature and reported the first fabricated virus, RaTG13. Since then, many virus fabrications have taken place and all of them were published as peer-reviewed articles on top scientific journals. Subsequently, based on such reports, influential opinion articles promoting the natural origin theory have then been published by prominent scientists and international organizations on such and other high-profile platforms.

In contrast to the rigorous promotion of the natural origin theory, strict censorship has been placed by these and other journals on manuscripts discussing a possible laboratory origin of SARS-CoV-2. Our earlier report, which was one of such manuscripts and published as a preprint article, also faced unfounded criticisms dressed as unbiased peer reviews from two groups of scientists led by Drs. Robert Gallo and Nancy Connell, respectively (our point-to-point responses are being prepared and will be published soon). As a result of this collaborative efforts, the public has been largely removed from the truth about COVID-19 and SARS-CoV-2, which has led to misjudgments, delayed actions, and greater sufferings of the global community. It is imperative to investigate the scientists, laboratories, institutions, and relevant collaborators responsible for the creation of SARS-CoV-2 and for the fabrications/cover-up.

It is also imperative to investigate the relevant individuals in the WHO, at the relevant scientific journals, in the relevant funding agencies, and in other relevant bodies, which have facilitated the creation of SARSCoV-2 and the scientific cover-up of its true origin while under full awareness of the nature of these operations. Finally, it also needs to be investigated which ones of the scientists engaged in the promotion of the natural origin theory were purely misled by the scientific fraud and which ones were colluding with the CCP government.

The time has come that the world faces the truth of COVID-19 and takes actions to save the future of humanity.

Acknowledgements

We thank Daoyu Zhang for sharing with us the observation of abnormal distribution of nonsynonymous mutations between RaTG13 Spike and SARS-CoV-2. We thank Francisco de Asis for revealing the filenames of the raw sequencing reads for RaTG13. We also thank other individuals, including anonymous scientists, for uncovering various facts associated with the origin of SARS-CoV-2.
 

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In Central Asia’s forbidding highlands, a quiet newcomer: Chinese troops

NEAR SHAYMAK, Tajikistan — Two miles above sea level in the inhospitable highlands of Central Asia, there’s a new power watching over an old passage into Afghanistan: China.
For at least three years, Chinese troops have quietly monitored this choke point in Tajikistan just beyond China’s western frontier, according to interviews, analysis of satellite images and photographs, and firsthand observations by a Washington Post journalist.

While veiled in secrecy, the outpost of about two dozen buildings and lookout towers illustrates how the footprint of Chinese hard power has been expanding alongside the country’s swelling economic reach.
Tajikistan — awash in Chinese investment — joins the list of Chinese military sites that includes Djibouti in the strategic Horn of Africa and man-made islands in the South China Sea, in the heart of Southeast Asia.
AD


Meanwhile, Chinese President Xi Jinping’s economic ambitions over the past seven years have brought a wave of major investment projects, from the resource-rich Caspian Sea to Cambodia’s coastline.
The modest facility in Tajikistan — which offers a springboard into Afghanistan’s Wakhan Corridor a few miles away — has not been publicly acknowledged by any government.
But its presence is rich in significance and symbolism.
Watch: U.S. Navy ship sails in disputed South China Sea
At a moment when the United States might consider a pact that would pull American troops out of Afghanistan, China appears to be tiptoeing into a volatile region critical to its security and its continental ambitions.
A map locating a military outpost in Tajikistan, near the Wakhan Corridor of Aghanistan

Already, the retreat of old powers and arrival of the new are on display in Tajikistan, a tiny, impoverished country that served as a gateway into Afghanistan for U.S. units in the early phases of the 2001 invasion.
AD


During a recent trip along the Tajikistan-Afghanistan border, The Post saw one of the military compounds and encountered a group of uniformed Chinese troops shopping in a Tajik town, the nearest market to their base. They bore the collar insignia of a unit from Xinjiang, the Chinese territory where authorities have detained an estimated 1 million Uighurs, a mostly Muslim ethnic minority.
The crackdowns against the Uighurs have been internationally condemned as a violation of human rights, but the Chinese government says they are part of a campaign to insulate its restive far west from Islamic extremism seeping in from Central Asia.
“We’ve been here three, four years,” a soldier who gave his surname as Ma said in a brief conversation while his Chinese comrades, guided by a Tajik interpreter, bought snacks and topped up their mobile SIM cards in Murghab, a sprawl of low-rises about 85 miles north of the base.
AD


When asked whether his unit had intercepted anyone crossing from Afghanistan, Ma smiled.
“You should be aware of our government’s policies about secrecy,” he said. “But I can say: It’s been pretty quiet.”
Scarce public information
Details about China’s activities at the facilities, some of which bear the Chinese and Tajik emblems, are not made public. Also unclear are the arrangements over their funding, construction and ownership. Satellite imagery shows what appear to be two clusters of buildings, barracks and training grounds, about 10 miles apart near the mouth of the Wakhan Corridor, a narrow strip of territory in northeastern Afghanistan.
A Chinese soldier with the surname Ma buys goods in the Murghab bazaar. He told The Post that Chinese forces have been in Tajikistan for three to four years.

A Chinese soldier with the surname Ma buys goods in the Murghab bazaar. He told The Post that Chinese forces have been in Tajikistan for three to four years. (Gerry Shih/The Washington Post)
The Post separately spoke to members of a German mountaineering expedition who said they were interrogated in 2016 by Chinese troops patrolling the Afghan corridor, near the settlement of Baza’i Gonbad. Photos provided by Steffan Graupner, the expedition leader, showed Chinese mine-resistant armored vehicles and equipment embossed with the country’s paramilitary logo. Taken together, the findings add weight to a growing number of reports that China, despite public denials, has been conducting security operations inside Afghanistan.
China’s military advances have Pentagon on edge
China’s Foreign Ministry declined to comment and directed questions to the Defense Ministry, which did not respond to requests for comment.
AD


In a statement, Tajikistan’s Foreign Ministry said there are “no People’s Republic of China military bases on the territory of the Republic of Tajikistan,” nor “any talks whatsoever” to establish one.
Analysts say the Chinese encountered by The Post may be paramilitary units under the command of the central military leadership but technically distinct from the People’s Liberation Army, China’s main war-fighting force.
U.S. officials say they are aware of the Chinese deployment but do not have a clear understanding of its operations. They say they do not object to the Chinese presence because the United States also believes that a porous Afghan-Tajik border could pose a security risk.
China’s encroachment into Afghanistan is “fascinating but not surprising — and should be welcomed by Washington,” said Ely Ratner, executive vice president at the Center for a New American Security, who was a deputy national security adviser to then-Vice President Joe Biden.
A satellite view of one of the Chinese outposts at the border between Tajikistan and Afghanistan on Sept. 29.

A satellite view of one of the Chinese outposts at the border between Tajikistan and Afghanistan on Sept. 29. (Planet Labs)
“We can and should foist more responsibility for Afghanistan on China,” Ratner said. “They don’t want a target on their back, but they’ve been free-riding on U.S. dollars and lives for security.”
Watch: U.S. general says China’s military rise is on all fronts
Despite harboring concerns about militants in Afghanistan for decades, China has been loath to be seen as siding with any party in the conflict, much less to put boots on the ground.
AD


Instead, China’s state-owned companies and banks have inked infrastructure deals, mining concessions and loans across Central and South Asia, the poor and turbulent belt that makes up its backyard. Its diplomats, who have robust ties with Afghanistan, Pakistan and the Taliban, have talked up China’s role as a regional peace broker — never a peacekeeper.
But China’s global posture is changing under Xi, who has shed the country’s long-standing isolationism and spoken loftily about restoring its great-power status.
People’s Liberation Army (PLA) strategists increasingly advocate for pushing beyond the Chinese mainland with deployments that follow in the wake of the country’s expanding “haiwailiyi,” or interests abroad, said Andrew Scobell, a Chinese security expert at the Rand Corp.

“China’s peaceful rise has encountered a complicated and severe situation,” Maj. Li Dong wrote in a 2016 journal article as part of a PLA assessment of China’s overseas military strategy. He pinpointed the Central Asian frontier as one of three top flash points along with the Korean Peninsula and the East and South China seas.
AD

China’s deployments abroad lack strength and “flexibility,” Li wrote. “China should push the construction of its overseas military presence gradually.”
A rugged chessboard
In 2017, China unveiled a naval base in Djibouti that gave it a foothold in the Middle East and Africa. It steadily installed infrastructure — and later, weaponry — in the contested South China Sea. A recent Pentagon report predicted a PLA base could appear soon in Pakistan — a prospect China has denied.
Chinese troops visit the Murghab bazaar.

Chinese troops visit the Murghab bazaar. (Gerry Shih/The Washington Post)
Beijing’s moves have been similarly opaque in the rugged mountains spanning Tajikistan, Afghanistan, Pakistan and China: the same chessboard where czarist Russia and the British Empire vied for influence 150 years ago.

There will be “no Chinese military personnel of any kind on Afghan soil at any time,” Col. Wu Qian, the Defense Ministry’s spokesman, told reporters in August.
Opinion: The awkward romance of China and Russia
In private, the Chinese tell a slightly different story.
AD

In late 2017, the Development Research Center, an influential think tank under China’s cabinet, invited a handful of Russian researchers to its central Beijing offices. In what was billed as a private seminar, the Chinese explained why China had a security presence in Tajikistan that extended into the Afghans’ Wakhan Corridor, according to Alexander Gabuev of the Carnegie Moscow Center, a Russian participant.
The Chinese researchers took pains to describe the outpost as built for training and logistical purposes — not a military occupation. They also sought to gauge Russia’s reaction with questions: How would Moscow view China’s move into its traditional sphere of influence? Would it be more palatable if China deployed private mercenaries instead of uniformed men?

“They wanted to know what Russia’s red lines were,” said Gabuev, who has held similar conversations with scholars working under the Chinese intelligence agency. “They don’t want Russia blindsided.”
AD

In the 1990s, a Uighur separatist group, calling itself the East Turkestan Independence Movement, rose in Afghanistan under the protection of the Taliban and threatened attacks against China. Although Western officials and analysts question the ETIM’s ability to carry out significant attacks, it heralded the beginning of an extremist threat facing China.
Since 2014, hundreds, or most likely thousands, of Uighurs have left China for Syria, and Chinese officials, like their Western counterparts, have warned about the prospect of fighters there decamping for Central Asia as they lose territory. In 2016, the Chinese Embassy in Kyrgyzstan was targeted in a suicide bombing that Kyrgyz authorities attributed to the al-Nusra Front in Syria.
'You never saw us here'
To make the days-long overland journey across Tajikistan, from the capital, Dushanbe, to the remote canyon held by Chinese soldiers, is to witness a landscape altered by an even more irrepressible force than the troops: Chinese money.
In the west, Chinese-built coal-fired plants loom over the skyline, providing electricity and heat to the capital’s residents. In the east, Chinese-funded hospitals and schools rise from the hardscrabble countryside. In the south, Chinese-financed tracks circumvent a crucial Soviet-era railway that had been shut down by Tajikistan’s neighbor, Uzbekistan. Stitching it all together are Chinese-bored tunnels and Chinese-laid asphalt that cut hours off trips along the country’s winding east-west highway.
Murghab, established as an army outpost in the 1890s by Russian Cossacks, is about 85 miles north of the remote Chinese border outpost.

Murghab, established as an army outpost in the 1890s by Russian Cossacks, is about 85 miles north of the remote Chinese border outpost. (Gerry Shih/The Washington Post)
The projects reflect Tajikistan’s strategic position in China’s Belt and Road Initiative, or BRI, an ambitious infrastructure investment plan to pull the Eurasian land mass into its economic embrace. China, through a single state bank, held more than half of Tajikistan’s external debt as of 2016, up from none in 2006, according to 2017 Tajik Finance Ministry data.
In the soft-power stakes, the United States and Russia both appear to be losing relative ground to China, which provides scholarships for undergraduate Tajiks and military academy training for up-and-coming defense officials.
Susan M. Elliott, former U.S. ambassador to Tajikistan, said China’s generous aid and funding should be applauded but viewed with skepticism. In the past year, a handful of countries that have taken Chinese investments have reconsidered BRI deals amid allegations of corruption and low feasibility.
China’s charm offensive in Asia
“If someone’s offering money to build roads and help put power lines up, it’s hard to turn that down when you have no alternative,” Elliott said. “This is a strategic and important part of the world, and we need to continue our strong partnerships with Tajikistan and other countries in the region.”
In many ways, the shifting geopolitical currents play out on the windy streets of Murghab, established as an army outpost in the 1890s by Russian Cossacks.
These days, it is Chinese troops who are dropping by in their unassuming minivans to pick up provisions.
Aiperi Bainazarova, a part-time manager at the only hotel in town, said locals believed there were scores, maybe hundreds, of Chinese troops who stayed on base. They mostly come to town to buy phone credit. Sometimes they buy hundreds of kilograms of yak meat at the price of 30 somoni — about $3 — a kilo, she said.
“It helps the economy,” said Bainazarova, 21, an ethnic Kyrgyz who studied on a Chinese government scholarship in Shanghai.
Despite the Chinese government’s insistence on keeping things secret, its troops’ periodic visits to Murghab’s bazaar, a row of shipping containers converted into storefronts, are anything but.
Safarmo Toshmamadov is a shopkeeper in Murghab. Some of her customers are Chinese troops.

Safarmo Toshmamadov is a shopkeeper in Murghab. Some of her customers are Chinese troops. (Gerry Shih/The Washington Post)
Safarmo Toshmamadov, a 53-year-old ethnic Pamir shopkeeper, said they have come to her for maybe three years. Some attempt a few words of Russian — although they always come accompanied by Tajik interpreters, she said.
“We don’t think about them, and they don’t bother us,” Toshmamadov said, shrugging. “They buy my water and snacks. It’s good.”
One afternoon outside Toshmamadov’s store, a Post reporter saw Ma, the Chinese soldier, who was initially surprised to encounter another Chinese speaker.
He spoke guardedly but affably about his deployment, which he explained was secret.
“You should know our government’s standard policies around revealing information,” he said. “So don’t tell your friends.”
When asked to pose for a photo together, Ma recoiled.
“Remember,” he said, walking away. “You never saw us here.”
 

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Chinese Whistleblower Li-Meng Yan Claims Coronavirus Lab Release Was in 'No Way an Accident' Amid Strict P3 and P4 Surveillance

Chinese Whistleblower Dr. Li-Meng Yan has been making headlines for alleging that the coronavirus actually came from a laboratory in Wuhan as opposed to the previous belief that the virus came from a wet market. Li-Meng Yan alleged that the virus was manufactured inside a laboratory and that her seniors all knew about the virus but chose to keep it a secret.
Li-Meng Yan's allegations
According to her reports, the virus could have been stopped if they did not keep the information a secret when there were only five positive cases to begin with. She alleged that the deadly virus was already released but they only acknowledged it when it was too late.

Dr. Yan announced that she has been treated harshly by the Chinese Communist Party and has even experienced cyber attacks. Dr. Yan's original social media account was previously deleted but she has been able to make a new Twitter account that has not yet been taken down.
Click to expand...
Just recently, Dr. Yan also alleged that her mother back in China was arrested by the Chinese Communist Party in an attempt to threaten and silence her. However, the Chinese virologist is still very firm about sharing her story in hopes that the truth will be revealed.
The virus could not have been released by accident?
In another recent video that went out just last week regarding Dr. Yan's coronavirus story, she revealed even more information about the events surrounding its release. According to her, the virus was intentionally released due to how strict the laboratory was and how impossible a mistake could have happened.
Dr. Li-Meng Yan described the working environment saying that the P3 lab, where she worked, as well as the P4 lab, was under strict protocols and they were all put under strict surveillance and that only employees have passes. It would have been impossible to sneak out the virus without being detected unless it was an inside job.
She stated that they all have 24 hour 7 days a week surveillance cameras within the lab so if someone were to smuggle the virus outside of the lab, they would have been caught. There was supposedly an exam that was taken and that all of the researchers supposedly went through strict training in order to make sure the team was filtered. She then stated that "there is no way for these kinds of accidents to be released."
Here is the newest article by Dr. Li-Meng Yan and other Chinese scientists proving that Covid-19 virus is a bioweapon created in a Chinese military lab, and intentionally leaked out to the world. I am not including the referenced figures and citations (due to format limitations); the full report (in pdf format) with all figures and citations can be accessed via this link:
SARS-CoV-2 Is an Unrestricted Bioweapon: A Truth Revealed through Uncovering a Large-Scale, Organized Scientific Fraud
Li-Meng Yan (MD, PhD), Shu Kang (PhD), Jie Guan (PhD), Shanchang Hu (PhD)
Rule of Law Society & Rule of Law Foundation, New York, NY, USA.

Correspondence: [email protected]

Abstract

Two possibilities should be considered for the origin of SARS-CoV-2: natural evolution or laboratory creation. In our earlier report titled “Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route”, we disproved the possibility of SARS-CoV-2 arising naturally through evolution and instead proved that SARS-CoV-2 must have been a product of laboratory modification. Despite this and similar efforts, the laboratory creation theory continues to be downplayed or even diminished. This is fundamentally because the natural origin theory remains supported by several novel coronaviruses published after the start of the outbreak. These viruses (the RaTG13 bat coronavirus, a series of pangolin coronaviruses, and the RmYN02 bat coronavirus) reportedly share high sequence homology with SARSCoV- 2 and have altogether constructed a seemingly plausible pathway for the natural evolution of SARSCoV-2. Here, however, we use in-depth analyses of the available data and literature to prove that these novel animal coronaviruses do not exist in nature and their sequences have been fabricated. In addition, we also offer our insights on the hypothesis that SARS-CoV-2 may have originated naturally from a coronavirus that infected the Mojiang miners.

Revelation of these virus fabrications renders the natural origin theory unfounded. It also strengthens our earlier assertion that SARS-CoV-2 is a product of laboratory modification, which can be created in approximately six months using a template virus owned by a laboratory of the People’s Liberation Army (PLA). The fact that data fabrications were used to cover up the true origin of SARS-CoV-2 further implicates that the laboratory modification here is beyond simple gain-of-function research.

The scale and the coordinated nature of this scientific fraud signifies the degree of corruption in the fields of academic research and public health. As a result of such corruption, damages have been made both to the reputation of the scientific community and to the well-being of the global community.

Importantly, while SARS-CoV-2 meets the criteria of a bioweapon specified by the PLA, its impact is well beyond what is conceived for a typical bioweapon. In addition, records indicate that the unleashing of this weaponized pathogen should have been intentional rather than accidental. We therefore define SARS-CoV-2 as an Unrestricted Bioweapon and the current pandemic a result of Unrestricted Biowarfare.

We further suggest that investigations should be carried out on the suspected government and individuals and the responsible ones be held accountable for this brutal attack on the global community.

Introduction

SARS-CoV-2 is a novel coronavirus and the causative agent of the COVID-19 pandemic. Despite its tremendous impact, the origin of SARS-CoV-2, however, has been a topic of great controversy. In our first report titled “Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route”, we used biological evidence and in-depth analyses to show that SARS-CoV-2 must be a laboratory product, which was created by using a template virus (ZC45/ZXC21) owned by military research laboratories under the control of the Chinese Communist Party (CCP) government. In addition, resources and expertise are all in place in the Wuhan Institute of Virology (WIV) and related, other CCP-controlled institutions allowing the creation of SARS-CoV-2 in approximately six months.

What have not been fully described in our earlier analyses are details of the novel animal coronaviruses published by the CCP-controlled laboratories after the outbreak1. While no coronaviruses reported prior to 2020 share more than 90% sequence identity with SARS-CoV-2, these recently published, novel animal coronaviruses (the RaTG13 bat coronavirus, a series of pangolin coronaviruses, and the RmYN02 bat coronavirus9) all share over 90% sequence identities with SARS-CoV-2. As a result, these SARS-CoV-2-like viruses have filled an evolutionary gap and served as the founding evidence for the theory that SARS-CoV-2 has a natural origin. In this report, we provide genetic and other analyses, which, when combined with recent findings, prove that these novel animal coronaviruses do not exist in nature and their genomic sequences are results of fabrication.

1. Evidence proving that the RaTG13 virus is fraudulent and does not exist in nature

On February 3rd, 2020, Dr. Zhengli Shi and colleagues published an article in Nature titled “A pneumonia outbreak associated with a new coronavirus of probable bat origin” (manuscript submitted on January 20th), which was one of the first publications to identify SARS-CoV-2 as the pathogen causing the disease now widely known as COVID-19. Also reported in this article was a novel bat coronavirus named RaTG13, the genomic sequence of which was shown to be 96.2% identical to that of SARS-CoV-2. The close evolutionary relationship between RaTG13 and SARS-CoV-2 as suggested by the high sequence identity had led to a conclusion that SARS-CoV-2 has a natural origin. These striking findings have consequently made this article one of the most cited publications in the currently overwhelmed field of coronavirus research. Interestingly, an article published by Dr. Yong-Zhen Zhang and colleagues on the same issue of Nature, which also discovered SARS-CoV-2 as the responsible pathogen for COVID-19, received much less citations. This latter article made no mention of RaTG13. Instead, Zhang and colleagues showed that, evolutionarily, SARS-CoV-2 was closest to two bat coronaviruses, ZC45 and ZXC21, both of which were discovered and characterized by military research laboratories under the control of the CCP government. Immediately after the publication of this article, Dr. Zhang’s laboratory was shut down by the CCP government with no explanations offered.

Since its publication, the RaTG13 virus has served as the founding evidence for the theory that SARSCoV-2 must have a natural origin. However, no live virus or an intact genome of RaTG13 have ever been isolated or recovered. Therefore, the only proof for the “existence” of RaTG13 in nature is its genomic sequence published on GenBank.

1.1 The sequence of RaTG13 uploaded at GenBank can be fabricated

In order to have the sequence of a viral genome successfully uploaded onto GenBank, submitters have to provide both the assembled genomic sequence (text only) and raw sequencing reads. The latter is used for quality control and verification purposes. However, due to the huge amount of work involved in assembling raw reads into complete genomes, no sufficient curation is in place to ensure the correctness or truthfulness of the uploaded viral genomes. Therefore, an entry on GenBank, which in this case is equivalent to the existence of an assembled viral genomic sequence and its associated sequencing reads, is not a definitive proof that this viral genome is correct or real.

Sequencing of a viral RNA genome requires amplifying segments of it using reverse transcriptase PCR (RT-PCR) as the first step. The products of the RT-PCR, which are double-stranded DNA, would subsequently be sent for sequencing. The resulted sequencing reads, each ideally revealing the sequence of a segment of the genome, are then used to assemble the genome of the virus under study (Figure 1A).

Typically, some segments of the genome may not be covered by the initial round of sequencing. Therefore, gap filling will be carried out, where these missing segments will be amplified specifically and the DNA products subsequently sequenced. These steps are repeated until a complete genome can be assembled, ideally with a proper depth to ensure accuracy.

However, this process leaves room for potential fraud. If one intends to fabricate an RNA viral genome on GenBank, he or she could do so by following these steps: create its genomic sequence on a computer, have segments of the genome synthesized based on the sequence, amplify each DNA segment through PCR, and then send the PCR products (may also be mixed with genetic material derived from the alleged host of the virus to mimic an authentic sequencing sample) for sequencing (Figure 1B). The resulted raw sequencing reads would be used, together with the created genomic sequence, for establishing an entry on GenBank. Once accomplished, this entry would be accepted as the evidence for the natural existence of the corresponding virus. Clearly, a viral genomic sequence and its GenBank entry can be fabricated if well-planned.

The complete genomic sequence of RaTG13 was first submitted to GenBank on January 27th, 2020. The raw sequencing reads were made available on February 13th, 2020 (NCBI SRA: SRP249482).

However, the sequencing data for gap filling, which is indispensable in assembling a complete genome, was only made available on May 19th, 2020 (NCBI SRA: SRX8357956). The timing and the reversed order of events here are strange and suspicious.

The raw sequencing reads of RaTG13 have multiple abnormal features. Despite the sample being described as a fecal swab, only 0.7% of the raw sequencing reads are bacterial reads while the bacterial abundance is typically 70~90% when other fecal swab samples were sequenced. In addition, in the identifiable region of certain sequencing reads, a vast majority of reads are eukaryotic sequences, which is also highly unusual in the sequencing of fecal swap-derived samples. Within these eukaryotic reads, 30% of the sequences are of non-bat origin and instead shown to be from many different types of animals including fox, flying fox, squirrels, etc. These abnormal features are significant and indicate that the raw sequencing reads should have been obtained via a route that is different from the normal one (Figure 1).

No independent verification of the RaTG13 sequence seems possible because, according to Dr. Zhengli Shi, the raw sample has been exhausted and no live virus was ever isolated or recovered. Notably, this information was known to a core circle of virologists early on and apparently accepted by them. It was then made public, months later, by Dr. Yanyi Wang, director general of the WIV, in an TV interview on May 23rd, 2020. Dr. Shi also confirmed this publicly in her email interview with Science in July 2020.

However, judging from Shi’s published protocol, exhaustion of the fecal swap sample is highly unlikely. According to this protocol, the fecal swab sample would be mixed with 1 ml of viral transport medium and the supernatant collected. Every 140 ul of the supernatant would then yield 60 ul of extracted RNA. For the subsequent step, RT-PCR, 5 ul of this RNA-containing solution is required per reaction.

Therefore, from one fecal swab sample, at least 80 RT-PCR reactions could be carried out ([1000/140] x 60/5=86). Such an amount is sufficient to support both the initial round of sequencing and the subsequent gap filling PCR. It would be sufficient to also allow reasonable attempts to isolate live viruses, although Dr. Shi claimed that no virus isolation was attempted.

Therefore, the RaTG13 virus and its published sequence are suspicious and show signs of fabrication.

1.2 Other suspicions associated with RaTG13

RaTG13 was reported by Dr. Zhengli Shi from the WIV. Dr. Shi is a fellow of the American Academy of Microbiology and one of the most accomplished Chinese virologists. A peer-reviewed article authored by her and published on the top journal Nature, therefore, brought a great level of comfort for the coronavirus research community in accepting RaTG13 as a true, nature-born bat coronavirus. As a result, RaTG13, upon its timely publication, served as the founding evidence for the natural origin theory of SARS-CoV-2.

However, as revealed in section 1.1, the reported sequence of RaTG13, which is the only proof of the virus’ existence in nature, is problematic and shows signs of fabrication.
Intriguingly, despite the pivotal role of RaTG13 in revealing the origin of SARS-CoV-2, the
information provided for its discovery was surprisingly scarce with key points missing (location and date of sample collection, previous knowledge and publication of this virus, etc):

We then found that a short region of RNA-dependent RNA polymerase (RdRp) from a bat coronavirus (BatCoV RaTG13)—which was previously detected in Rhinolophus affinis from Yunnan province—showed high sequence identity to 2019-nCoV. We carried out full-length sequencing on this RNA sample (GISAID accession number EPI_ISL_402131). Simplot analysis showed that 2019-nCoV was highly similar throughout the genome to RaTG13 (Fig. 1c), with an overall genome sequence identity of 96.2%.

Only in the source section of the NCBI entry for RaTG13 (GenBank accession code: MN996532.1), one could find that the original sample was a “fecal swab” collected on “July 24th, 2013”. A closer look at the sequence reveals that RaTG13 shares a 100% nucleotide sequence identity with a bat coronavirus RaBtCoV/4991 on a short, 440-bp RNA-dependent RNA polymerase gene (RdRp) segment.

RaBtCoV/4991 was discovered by Shi and colleagues and published in 2016. As described in the 2016 publication, only a short 440-bp segment of RdRp of the RaBtCoV/4991 virus was sequenced then. Given the 100% identity on this short gene segment between RaBtCoV/4991 and RaTG13, the field has demanded clarification of whether or not these two names refer to the same virus. However, Dr. Shi did not respond to the request or address this question for months. The answer finally came from Peter Daszak, president of EcoHealth Alliance and long-term collaborator of Shi, who claimed that RaBtCoV/4991 was RaTG13.

RaBtCoV/4991 was discovered in the Yunnan province, China. In 2012, six miners suffered from severe pneumonia after clearing out bat droppings in a mineshaft in Mojiang, Yunnan, and three of them died soon afterwards. Although it was initially suspected that a SARS-like bat coronavirus may be responsible for the deaths, no coronavirus was either isolated or detected from the clinical samples. Also, first-hand record indicates failure of biopsy and no attempt of autopsy, which are the gold standards in the diagnosis of coronavirus infections. The pathogen responsible for the miners’ deaths therefore remained an unsolved case. (Detailed analyses of the Mojiang Miner Passage hypothesis, which was based on the miners’ case, are provided in section 1.6.) Despite the failed diagnosis, this unknown pathogen nonetheless triggered immense interests in the virologists in China. Three independent teams, including that of Dr. Shi’s, made a total of six visits to this mineshaft. The Shi group particularly looked for the presence of bat coronaviruses by amplifying and then sequencing a 440-bp RdRp segment, which is a routine procedure the Shi group follows in their surveillance studies. (As shown in section 2.1 of our first report, this RdRp segment is also frequently used for phylogenetic analyses and is an attractive target for antiviral drug discovery, which may have contributed to the design of incorporating a unique RdRp into the genome of SARS-CoV-2.) Out of the many coronaviruses detected, only RaBtCoV/4991 seemed to belong to the group of SARS-related, lineage B β coronaviruses.

The reporting of RaTG13 is suspicious in three aspects.

First, the whole genome sequencing of RaBtCoV/4991 should not have been delayed until 2020. Given the Shi group’s consistent interests in studying SARS-like bat coronaviruses and the fact that RaBtCoV/4991 is a SARS-like coronavirus with a possible connection to the deaths of the miners, it is highly unlikely that the Shi group would be content with sequencing only a 440-bp segment of RdRp and not pursue the sequencing of the receptor-binding motif (RBM)-encoding region of the spike gene. In fact, sequencing of the spike gene is routinely attempted by the Shi group once the presence of a SARS-like bat coronavirus is confirmed by the sequencing of the 440-bp RdRp segment, although the success of such efforts is often hindered by the poor quality of the sample.

As quoted above, in the 2020 Nature publication, Shi and colleagues strongly suggested that the sequencing of the full genome was done in 2020 after they discovered the resemblance between RaTG13 and SARS-CoV-2 on the short RdRp segment4. This, if true, suggests that the quality of the sample should not be poor. Therefore, there is no technical obstacle for the whole genome sequencing of RaBtCoV/4991.

Clearly, the perceivable motivation of the Shi group to study this RaBtCoV/4991 virus and the fact that no genome sequencing of it was done for a period of seven years (2013-2020) are hard to reconcile and explain.

However, an intriguing revelation took place in June 2020. Specifically, filenames of the raw sequencing reads for RaTG13 uploaded on the database were found, which indicate that these sequencing experiments were done in 2017 and 2018. Likely responding to this revelation, in her email interview with Science, Dr. Shi contradicted her own description in the Nature publication and admitted that the sequencing of the full genome of RaTG13 was done in 2018.

Second, RaTG13 has a remarkable RBM as suggested by its reported sequence, and the Shi group have no reason to delay its publication until 2020. The most critical segment of a SARS-like β coronavirus is the RBM in the Spike protein as it is fully responsible for binding the host ACE2 receptor and therefore determines the virus’ potential in infecting humans. The RBM is also the most variable region because it is under strong positive selection when the virus jumps over to a new host. Sequence alignment on this crucial RBM motif reveals that the RaTG13 virus rivals with the most highly regarded bat coronaviruses in terms of resemblance to SARS (Figure 2). RaTG13’s RBM not only is complete in reference to that of SARS but also is outstanding in its preservation of five residues perceived by Dr. Shi as key in binding human ACE2 (hACE2) (Figure 2, residues labeled with red texts). At position 472, RaTG13 is the only bat coronavirus that shares a leucine (L) residue with SARS, while the other four key residues are also largely conserved between the two viruses. Importantly, similar conservation patterns revealed in related bat coronaviruses, Rs3367 and SHC014, had led to their publication in Nature in 2013. Furthermore, viruses with less “attractive” RBM sequences (having large gaps and poor in the preservation of key residues, bottom half of the sequences in Figure 2) were also published by Dr. Shi in other top virology journals between 2013 and 2018. Therefore, if the genomic sequence of RaTG13 had been available since 2018, it is unlikely that this virus, which has a possible connection to miners’ deaths in 2012 and has an alarming SARS-like RBM, would be shelfed for two years without publication. Consistent with this analysis, a recent study indeed proved that the RBD of RaTG13 (produced via gene synthesis based on its published sequence) was capable of binding hACE2.

Third, no follow-up work on RaTG13 has been reported by the Shi group. Upon obtaining the genomic sequence of a SARS-like bat coronavirus, the Shi group routinely investigate whether or not the virus is capable of infecting human cells. This pattern of research activities has been shown repeatedly.

However, such a pattern is not seen here despite that RaTG13 has an interesting RBM and is allegedly the closest match evolutionarily to SARS-CoV-2.

Clearly, these three aspects deviate from normal research activities and logical thinking, which are difficult to reconcile or explain. They should have contributed to the intentional omission of key information in the reporting of RaTG13.

For publications of biological research, it is unethical for authors to change the name of a previously published virus without any notice or description. It is also unethical for authors to not cite their own

publication where they had characterized and reported the same virus. The violations here by Shi and colleagues on the reporting of RaTG13 are especially aggravating as the discovery of RaTG13 was central to uncovering the origin of SARS-CoV-2. By the time of the publication, SARS-CoV-2 had already led to many deaths in the city of Wuhan and had shown an alarming potential of causing a pandemic. In her much-delayed response to Science published on July 31st, 2020, Dr. Shi finally commented on the name change and stated that changing the name to RaTG13 was meant to better reflect the time and location of sample collection (TG = Tongguan; 13 = 2013). However, such an intention does not seem to justify why the previous name of RaBtCoV/4991 was never mentioned in the 2020 article and why they did not cite their own 2016 publication where RaBtCoV/4991 was first reported. Dr. Shi’s recent clarification did not alter the fact that they have violated the reporting norms of biological research.

In summary, a range of suspicions were associated with the reporting of RaTG13, including the violations of scientific publication principles, the inconsistency in the descriptions of the sequencing dates, and the contradiction between the sequencing of its genome in 2018 and the publication of it in 2020 when this virus has a striking RBM and a possible connection to pneumonia-associated deaths. Adding to these suspicions are the exquisite timing of its publication, the problematic nature of its reported sequence and raw sequencing reads, and the claim that no sample is left for independent verification. Collectively, these facts justify and legitimate the concern over the true existence of the RaTG13 virus in nature and the truthfulness of its reported genomic sequence. They also question the claim that the RaBtCoV/4991 virus and RaTG13 are equivalent.

1.3 Genetic evidence proving the fraudulent nature of RaTG13

This evidence was revealed after a close examination of the sequences of specific genes, especially spike, of relevant viruses. Specifically, we compared two viruses for the synonymous and nonsynonymous mutations on each gene, and we did so for two pairs of viruses. The first pair are bat coronaviruses ZC45 and ZXC21. The second pair are SARS-CoV-2 and RaTG13. The rationale for comparing these two pairs with each other is the following. First, ZC45 and ZXC21, each sharing an 89% genomic sequence identity with SARS-CoV-2, are the closest relatives to SARS-CoV-2 and RaTG13.

Second, ZC45 and ZXC21 are 97% identical to each other, while SARS-CoV-2 and RaTG13 are 96% identical. Not only the sequence identity in each case is comparable, but also the high sequence identity indicates that, within each pair, the sequence difference should be a result of random mutations during evolution, which ensures that synonymous and non-synonymous analyses here are appropriate and not complicated by abrupt evolutionary events (e.g. recombination). Indeed, sequence alignment confirms such a scenario – in both cases, the curve is smooth and the high sequence identity is maintained
throughout (Figure 3).

Detailed synonymous (syn, green curve) and non-synonymous (non-syn, red curve) analyses are shown in Figure 4. For each gene, the accumulations of syn and non-syn mutations, respectively, are illustrated when the codons are analyzed in a sequential order. For the spike genes, between ZC45 and ZXC21, the syn/non-syn ratio is 5.5:1 (Figure 4A left, 94 syn mutations and 17 non-syn mutations). Notably, the two curves progress along in a roughly synchronized manner. These features reflect, to a certain extent, the evolutionary traits resulted from random mutations during evolution in this sub-group of lineage B β coronaviruses.

The same analysis on the spike genes of SARS-CoV-2 and RaTG13, however, revealed a different scenario (Figure 4B right). Although the overall syn/non-syn ratio is a similar 5.4:1 (221 syn mutations and 41 non-syn mutations), the synchronization between the two curves is non-existent. In the second half of the sequence, which is over 700 codons (2,100 nucleotides) wide, the non-syn curve stays flat when the syn curve climbs continuously and significantly.

Counting the syn and non-syn mutations of the S2 region (corresponding to residues 684-1273 of the SARS-CoV-2 Spike) reveals that, between ZC45 and ZXC21, there are a total of 27 syn mutations and 5 non-syn mutations, yielding a syn/non-syn ratio of 5.4:1. In contrast, for the same S2 region, between SARS-CoV-2 and RaTG13, there are a total of 88 syn mutations and 2 non-syn mutations, yielding a syn/non-syn ratio of 44:1. The syn/non-syn ratios for S2, whole Spike, and other large viral proteins (Orf1a, Orf1b, and Nucleocapsid) are summarized in Table 1. While the ratios are comparable between the two groups for all other proteins, the ratios for the S2 protein are significantly different.

The detailed syn/non-syn analyses for Orf1a, Orf1b, and N are shown in Figure 4B-D. It is also noteworthy that, similar to that of Spike, the approximate synchronization between two curves is observed for the Orf1a protein in the ZC45 and ZXC21 comparison (Figure 4B left) but not in the SARS-CoV-2 and RaTG13 comparison (Figure 4B right).

The S2 protein maintains trimmer formation of the Spike and, upon successive cleavages to expose the fusion peptide, mediates membrane fusion and cell entry. Although the S2 protein is more conserved evolutionarily than S1, the extremely high purifying pressure on S2 as suggested by the very high syn/nonsyn ratio is abnormal. In fact, Orf1b is known to be the most conserved protein in coronaviruses and yet the syn/non-syn ratio for it is only 10.8:1 when SARS-CoV-2 and RaTG13 are compared, much lower than the ratio of 44:1 observed for S2 (Table 1). Furthermore, since RaTG13 and SARS-CoV-2 infect different species, no high purifying selection on S2 should be expected when these two viruses are compared against each other.

Consistent with the above notion, a syn/non-syn analysis done for the Spike protein of twenty randomly selected SARS-CoV-2 sequences showed that S2 was under positive selection, not purifying selection, during the past eight months of human-to-human transmission (Figure 5). For the twenty SARS-CoV-2 isolates, amino acid mutations are observed at five different locations in S2 (Figure 6). In addition, a recent study analyzing 2,954 genomes of SARS-CoV-2 revealed that mutations have been observed at 25 different locations in the S2 protein41, further proving that amino acid mutations are tolerated in S2 and no high purifying pressure should be observed for S2. Evidently, the syn/non-syn ratio of 44:1 revealed between SARS-CoV-2 and RaTG13 on the S2 region is abnormal (Table 1) and a violation of the principles of natural evolution.

A logical interpretation of this observation is that SARS-CoV-2 and RaTG13 could not relate to each other through natural evolution and at least one must be artificial. If one is a product of natural evolution, then the other one must be not. It is also possible that neither of them exists naturally.

If RaTG13 is a real virus that truly exists in nature, then SARS-CoV-2 must be artificial.

However, the reality is that SARS-CoV-2 is physically present and has first appeared prior to the reporting of RaTG13. This would then lead to the conclusion that RaTG13 is artificial, a scenario consistent with the overwhelming suspicion that this virus does not exist in nature and its sequence has been fabricated.

The remaining possibility is, of course, that both SARS-CoV-2 and RaTG13 are artificial: one has been created physically and the other one exists only in the form of a fabricated sequence.

It is highly likely that the sequence of the RaTG13 genome was fabricated by lightly modifying the SARS-CoV-2 sequence to achieve an overall 96.2% sequence identity. During this process, much editing must have been done for the RBM region of the S1/spike because the encoded RBM determines the interaction with ACE2 and therefore would be heavily scrutinized by others. An RBM too similar to that of SARS-CoV-2 would be troublesome because: 1) RaTG13 could be conceived as a product of gain-of-function research; 2) it would leave no room for an intermediate host and yet such a host is believed to exist as the Spike/RBM needs to first adapt in an environment where the ACE2 receptor is homologous to hACE2. In addition, modifying the sequence of the RBM is also beneficial as RaTG13 would otherwise appear to be able to infect humans as efficiently as SARS-CoV-2 does, escalating the concern of a laboratory leak. To eliminate such concerns, many non-syn mutations were introduced into the RBM region.

Importantly, syn/non-syn analysis is frequently used, often at the ORF/protein level, to characterize the

evolutionary history of a virus. While editing the RBM, the expert(s) carrying out this operation must be conscious of the need to maintain a reasonable syn/non-syn ratio for the whole Spike protein. To achieve so, however, the expert(s) must have then strictly limited the number of non-syn mutations in the S2 half of Spike, which ended up flattening the curve (Figure 4A right).

1.4 The receptor-binding domain (RBD) of RaTG13 does not bind ACE2 of horseshoe bats

Consistent with the above conclusion that RaTG13 does not exist in nature and its sequence was fabricated, a recent study showed that the RBD of RaTG13 could not bind the ACE2 receptors of two different kinds of horseshoe bats, Rhinolophus macrotis and Rhinolophus pusillus. Although the ACE2 receptor of Rhinolophus affinis (the alleged host of RaTG13) was not tested, it is unlikely that ACE2 of R. affinis would differ significantly from those of its close relatives and be able to bind the RaTG13 RBD.

This result therefore implicates that RaTG13 would not be able to infect horseshoe bats, contradicting the claim made by Shi and colleagues that the virus was detected and discovered from horseshoe bats. This is also consistent with the above conclusion that the genomic sequence of RaTG13 is fabricated and presumably computer-edited, which entails that the RBM/RBD suggested by the corresponding gene sequence may not be functional in binding the ACE2 receptor of the claimed host.

1.5 Conclusion and postulation of the fabrication process

In conclusion, the evidence presented both here and from recent literature collectively prove that RaTG13 does not exist in nature and its sequence has been fabricated.
If the RaBtCov/4991 virus is equivalent to RaTG13, then RaBtCoV/4991 must be fraudulent as well.

Apparently, in the actual process of sequence fabrication, the published sequence of the short RdRp segment of RaBtCoV/4991 was completely inherited for RaTG13. This way, they could claim that RaTG13 was RaBtCoV/4991, which, according to the record, was discovered in 2013. If RaTG13 had been described as being discovered right around the time of the COVID-19 outbreak, greater suspicions would result as tracing the evolutionary origin of a zoonotic virus is difficult and usually takes years or
decades. As described in section 2.1 of our earlier report1, the fabrication of RaTG13 should have been planned and executed in coordination with the laboratory creation of SARS-CoV-2.

Such an approach is also safe because, except for the 440-bp RdRp segment, no other sequence information has ever been published for the rest of the RaBtCoV/4991 genome.

It is worth noting that, due to reasons detailed in section 1.2, they still preferred to obscure the history of RaTG13. However, they must have also anticipated that their violations of the publication norms would invite inquiries or requests for clarifications, the number of which, however, should be limited and manageable. RaBtCoV/4991 would then function as an additional layer of security for them in facing such inquiries and/or requests.

Building upon the 440-bp RdRp sequence inherited from RaBtCoV/4991, the rest of the RaTG13 genome was likely fabricated by lightly editing the sequence of SARS-CoV-2. Once the genomic sequence was finalized, DNA fragments could be synthesized individually according to the fabricated and edited sequence and then used as templates for PCR. Amplified DNA would then be mixed with certain raw material to give the sample a natural look (mimicking what is present in an actual RT-PCR, which is done using RNA extracted from fecal swabs as templates). Subsequently, this sample would be sent for sequencing. The resulted raw sequencing reads could then be uploaded together with the made-up genomic sequence onto GenBank to create an entry for the RaTG13 genome.

1.6 The Mojiang Miner Passage (MMP) hypothesis is fatally flawed

Recently, a theory has emerged, which proposed that SARS-CoV-2 was derived from viral passaging in the lungs of the infected Mojiang miners back in 2012. Specifically, authors believe that the RaBtCoV/4991 virus was indeed RaTG13 and was the virus causing pneumonia in the miners in 2012.

While inside the lungs of the miners, the RaTG13 virus had evolved extensively, mimicking a viral passage process, and eventually became SARS-CoV-2. In this process, the RBD of the virus experienced strong positive selection, through which it became optimal in binding hACE2. Furthermore, the furin cleavage site at the S1/2 junction region of Spike had been acquired through recombination between the viral spike gene and the gene encoding the human ENaC protein, which has a furin-cleavage sequence closely resembling that of SARS-CoV-2. The end product of this passage was SARS-CoV-2, which the researchers isolated from the miners’ samples and brought back to the WIV. The authors have named this hypothesis as the Mojiang Miner Passage (MMP) hypothesis.

However, this MMP hypothesis has fatal flaws.

First, the viral pathogen that caused the disease in the miners could not be defined or confirmed.

According to the record, which was well documented in a Master’s Thesis written by the doctor in charge, samples from two patients (throat swabs and blood) were tested at the Center for Disease Control and Prevention of the Chengdu Military Region between May 15th and May 20th, 2012, and yet none of the suspected viruses, including SARS, was detected. Furthermore, the gold standard in the clinical diagnosis of coronavirus-caused pneumonia is biopsy and/or autopsy followed by confirmation by either RT-PCR or isolation of the virus. However, three biopsy tests were attempted but failed. Autopsy tests were requested and yet all turned down by families of the deceased miners. Due to such failure, both the Master’s Thesis and later a PhD Dissertation, which also looked into this issue although in an indirect manner, described the cause of the pneumonia as an unsolved case.

Second, antibody tests done for the miners do not support SARS or SARS-like coronavirus infection.

According to the Master’s Thesis, samples from two miners were tested for antibodies against SARS.

The symptoms onset date for one miner (case 3, passed away) was around April 13th, 2012. The other miner (case 4, had severe symptoms and yet recovered) had symptoms onset around April 16th, 2012.

Antibody tests, which were recommended later by Dr. Nanshan Zhong, were done at the WIV on June 19th, 2012. However, the two samples tested were only positive for IgM. No positive IgG or total antibody were reported. No antibody titer was reported either. Importantly, if the severe pneumonia was caused by coronavirus infections, by the time of the antibody tests on June 19th, 2012, both IgM and IgG/total antibody should be detected. In fact, IgG/total antibody should be much more abundant and easier to detect. On the other hand, IgM tests frequently result in false positives. Therefore, the fact
that only IgM, and no IgG/total antibody, was tested positive suggests that the described results were most likely false positives and the infections should not have been caused by SARS or a SARS-like coronavirus.

It is noteworthy that the later PhD Dissertation showed severe discrepancies with the Master’s Thesis in the descriptions of the same clinical tests:

1. The PhD Dissertation described that samples from four miners (throat swab and blood) were sent to the Center for Disease Control and Prevention of the Chengdu Military Region for nucleic acid tests. However, the Master’s Thesis indicated that samples were only taken from two miners.

2. The PhD Dissertation described samples from four miners were tested for anti-SARS antibodies at the WIV and all were IgG positive. However, the Master’s Thesis indicated that only samples from two miners were tested at the WIV and both were only IgM positive.

Importantly, the Master’s Thesis was written in 2013 in Yunnan by the doctor who was in charge of the six hospitalized miners. The PhD dissertation, however, was written in 2016 in Beijing based only on the clinical record. The author of the Dissertation had no direct involvement in the treatment of the miners or in any of the described tests. It is therefore highly likely that author of the PhD dissertation did not verify the clinical data he presented, which makes this PhD dissertation an unreliable source of information concerning the Mojiang miners’ case.

Third, if SARS-CoV-2 was already present in the miner’s body in 2012, it would have certainly caused an epidemic or even pandemic then. Given the extremely high transmissibility of SARS-CoV-2, it would be impossible for the doctors, nurses, family members of the miners, etc. to have avoided contracting the virus without the protection of proper PPE. If an epidemic indeed happened in 2012, it could not have gone unnoticed given the high transmissibility and lethality (three out of the six pneumonia patients died despite of intense medical care provided for them).

Fourth, as shown in sections 1.1-1.5, RaTG13’s sequence is clearly fabricated and the virus does not exist in nature. The RaBtCoV/4991 virus, which was detected in 2013, is not the RaTG13 virus that is defined by its reported genomic sequence. No complete genomic sequence of RaBtCoV/4991 has ever been reported likely due to the poor quality of the sample, which happens often as the RNA genome decays easily. It is highly likely that no high homology is shared between the actual RaBtCoV/4991 virus and SARS-CoV-2. This judgement is based on the fact that no viruses reported prior to 2020 share more than 90% sequence identity with SARS-CoV-2 despite the extensive surveillance studies of coronaviruses for the past two decades. Therefore, even if RaBtCoV/4991 was the pathogen responsible for the pneumonia of the miners, the theory that it has evolved in a single person’s lung into SARS-CoV-2 is far beyond being reasonable.

Fifth, it is impossible for the Spike protein of the virus to obtain a unique furin-cleavage site at the S1/S2 junction through recombination with the gene encoding the ENaC protein of the host cell (ENaC carries a furin cleavage site closely resembling the one seen in SARS-CoV-2). This is because recombination requires a significant level of sequence similarity between the two participating genes and yet no such similarity is present between coronavirus Spike and human ENaC. The molecular basis for recombination is non-existent. (Although recombination between ENaC and coronavirus Spike is impossible, it is suspicious that a viral protein and a host protein would share the same sequence for their furin-cleavage sites. It is possible, though, that the sequence of the furin-cleavage site in ENaC, which is known since 1997, could have been used in the design of the furin-cleavage site in the Spike of SARSCoV-2. Such a design may be considered sophisticated as ENaC co-expresses with ACE2 in many different types of cells.)

Sixth, if SARS-CoV-2 has indeed evolved from RaBtCoV/4991 in the miner’s lungs, it would look, from every aspect, like a naturally occurring virus. In that case, there would be no need to commit sequence fabrication for RaTG13 and for the other novel coronaviruses (parts 2 and 3) to falsify a natural origin for SARS-CoV-2.

Finally, as revealed in our earlier report, evidence exists in the genome of SARS-CoV-2, indicating that genetic manipulation is part of the history of SARS-CoV-2.

2. Evidence proving that recently published pangolin coronaviruses are fraudulent and do not exist in nature

While RaTG13 was reported to share a high sequence identity with SARS-CoV-2 and thereby hinted a natural origin of SARS-CoV-2, significant questions remained unanswered:

• No intermediate host has been found although one was believed to exist and function as the reservoir of the virus before it spilled over to humans.

• Despite the overall genomic resemblance of the two viruses, the RBD (particularly the RBM within it) of RaTG13 differs significantly from that of SARS-CoV-2. The evolutionary origin of the SARS-CoV-2 RBD, which is optimal in binding hACE2, remained unclear.

• A critical furin-cleavage site, which is present at the S1/S2 junction of SARS-CoV-2 Spike and responsible for the enhanced viral infectivity and pathogenicity, is absent in RaTG13 (as well as in all known lineage B β coronaviruses). The evolutionary origin of this furin-cleavage site also remained mysterious.

Not long after these questions emerged, several laboratories published novel coronaviruses allegedly found in Malayan pangolins that were smuggled from Malaysia and confiscated by the Chinese custom. Although these novel coronaviruses share relatively lower overall sequence identities (~90%) with SARS-CoV-2 in comparison to RaTG13 (96.2% identical to SARS-CoV-2), the RBD of the pangolin coronaviruses resembles greatly the SARS-CoV-2 RBD (97.4% identical). In the most critical RBM
region, all amino acids except one are identical between the pangolin coronaviruses and SARS-CoV-2.

These observations led the authors to conclude 1) that pangolins are the likely intermediate host for the zoonotic transfer of SARS-CoV-2 and 2) that a RaTG13-like ancestor coronavirus might have acquired the RBD from a pangolin coronavirus through recombination to eventually become SARS-CoV-2.

Here, in part 2 of the report, we describe literature evidence and provide genetic analyses to prove that these novel pangolin coronaviruses are results of fabrication.

2.1 A single batch of pangolin samples were used in all studies and the deposited sequencing data showed heavy contamination and signs of fabrication

In October 2019, a team formed by three researchers from two institutions (Guangdong Institute of Applied Biological Resources and Guangzhou Zoo) reported, for the first time, the detection of coronavirus infections in pangolins that were allegedly smuggled from Malaysia and confiscated in the Guangdong province in March 2019. Twenty-one pangolin samples were sequenced and five were positive for coronavirus infections (Table 2: lung 2, 7, 8, 9, and 11), although Sendai virus infection was also reported. However, neither the sequences of the coronaviruses nor raw sequencing data were made available to the public for a period of three months. The raw data (NCBI BioProject PRJNA573298) was finally released on January 22nd, 2020 after the COVID-19 outbreak started, while the article submission date was September 30th, 2019 and the publication date was October 24th, 2019.

Between March and May 2020, four seemingly independent studies were published, all of which reported novel pangolin coronaviruses and their assembled genomic sequences. However, after a closer look, we found that all four studies derived viral sequences from the same set of pangolin samples first reported in the October 2019 publication, which has been confirmed by a recent article.

In one study, Liu et al. (the same authors of the October 2019 publication) re-assembled the genome of a pangolin coronavirus by pooling two samples from the original 2019 study and one sample obtained from another Malayan pangolin rescued in July 2019. However, although the authors stated that the more recent raw sequencing data had been deposited at the NCBI database, we could not find this data using the accession number (2312773) provided. The same difficulty has been reported by others. Therefore, it cannot be verified whether the July 2019 dataset truly exists and has contributed to the assembly of the reported genome.

In two other studies, Lam et al. and Zhang et al. each re-assembled the genome of a pangolin coronavirus using only the published dataset from the October 2019 study. Lam et al. also reported detection of coronaviruses from smuggled Malayan pangolins that were confiscated in the Guangxi province, although these viruses showed lower sequence identities to SARS-CoV-2 both at the whole genome level (~86%) and in the critical RBD region. It is noteworthy that this study was done as a collaboration between Dr. Yi Guan’s group from the University of Hong Kong and Dr. Wuchun Cao’s group from the Academy of Military Medical Sciences (AMMS), Beijing, China. Somehow, all authors affiliated with the AMMS were excluded from the list of authors when the article was first submitted, although their names eventually appeared in the final version of the publication.

In the fourth study, Xiao et al. claimed to have examined tissue samples kept from diseased pangolins and obtained raw sequencing data for the subsequent assembly. However, they did not describe how the samples were acquired. In their Extended Data Table 3, they listed the metagenome sequencing data used in the study, which, surprisingly, do not match with the actual data that they uploaded in the database (Table 2). Samples M1, M5, M6, M10, and Z1 can be found in the data they deposited, but not M2, M3, M4, and M8. Furthermore, Xiao et al. apparently were inconsistent with the reporting of these raw sequencing reads. For samples M1, M6, pangolin3, and pangolin5, they counted paired ends numbers, which reflect the actual number of sequenced DNA fragments in the library. For the rest of samples, the authors counted reads numbers instead (In Illumina sequencing, there are two reads per fragment). For samples M2, M3, M4, and M8 in this latter group, when the reads numbers were converted to paired ends numbers (divided by 2), they each match perfectly with lung07, lung02, lung08, and lung11, respectively, from the October 2019 study (Table 2). Clearly, Xiao et al. used the data published in a previous study but failed to disclose this necessary information in their publication. In fact, they intentionally presented the “number of reads” in a different format to presumably make readers overlook the fact that the same sequencing dataset was used.

It is noteworthy that the study by Xiao et al. was also done in collaboration with the AMMS. Prior to the publication of the manuscript, this work was first publicized in a press conference. As revealed in this conference, four principle investigators contributed to the work and one of them was Dr. Ruifu Yang from the AMMS. However, like what happened to Dr. Cao and his AMMS colleagues in the Lam et al. study, Dr. Yang’s name was excluded in the submitted manuscript of Xiao et al. Yet, unlike the other case, the AMMS researcher’s name did not re-appear in the final publication. It is also noteworthy that the two AMMS principle investigators here, Dr. Yang and Dr. Cao, are long-term collaborators and most of their collaborative work concerned genetic analyses of SARS-CoV.

Among the four studies, only two assembled complete genomes by performing gap filling using PCR.

However, neither group made their gap filling sequences available, rendering independent verification impossible. Notably, the delayed publishing of raw sequencing reads long after the publication of genomic sequences has occurred in the reporting of RaTG13 as well.

Adding to the above problems was the poor quality of the raw sequencing data, which has been described recently. We also analyzed the composition of the sequencing reads of the deposited libraries. By performing taxonomy analysis on the NCBI SRA database, we also found that samples from Liu et al. that are positive for coronavirus reads are all positive for reads that map to human genome (Table 2). In great contrast, the rest of the samples, which are negative for viral reads, also have no human reads detected. The same correlation is found in data presented by Xiao et al. Although samples M5 (pangolin 6) and M6 (pangolin2) are negative for human reads, these two samples have very few viral reads, which would hardly contribute to the viral genome assembly. Clearly, the human contamination should not be due to sample handling as none of the coronavirus-negative samples, which must have been handled similarly, contain such contamination. The consistent co-existence of viral reads and human reads are highly suspicious.

These observations raise red flags not only on the credibility of the assembled sequences but also on the authenticity of these novel pangolin coronaviruses. It is also noteworthy that the manuscript submission dates for all four studies were between February 7th and February 18th, suggesting that their publications might have been coordinated.

2.2 No coronavirus was detected in an extensive surveillance study of Malayan pangolins

While these SARS-CoV-2-like pangolin coronaviruses were described as being detected in smuggled Malayan pangolins, a recent study strongly refuted the presence of such pangolin coronaviruses in nature.

A team led by Dr. Daszak examined 334 pangolin samples, which were collected in Malaysia and Sabah from August 2009 to March 2019. Surprisingly, no coronaviridae, or any of the other families of viruses (filoviridae, flaviviridae, orthomyxoviridae, and paramyxoviridae), were detected in any of these samples.

This is in stark contrast with the October 2019 publication where both coronavirus infection and Sendai virus infection were reportedly detected in the smuggled Malayan pangolins, which eventually led to the discovery and publication of the novel pangolin coronaviruses. The finding of Lee et al. adds significantly to the existing suspicions and substantiates the possibility that these pangolin coronaviruses do not exist in nature and their sequences could have been fabricated.

2.3 The RBD of the reported pangolin coronaviruses binds poorly to pangolin ACE2

If pangolin coronaviruses truly exist and have recently spilled over to infect humans, their Spike protein, especially the RBD within Spike, should bind to pangolin ACE2 (pACE2) more efficiently than to hACE2.

However, recent findings have contradicted this theory. In an in silico study, Piplani et al. calculated, following homology structural modeling, the binding energies involved in the association between SARSCoV-2 Spike and ACE2 from either human or various animals. Interestingly, the most favorable interaction that SARS-CoV-2 Spike makes was shown to be with hACE2, but not with ACE2 from pangolin or any other suspected intermediate host. Furthermore, another study revealed, using a robust in vitro binding assay, that the RBD of SARS-CoV-2 binds much tighter (greater than 9-fold) to hACE2 than to pACE2. Although the RBD of the pangolin coronaviruses is not 100% identical to that of SARSCoV-2, the RBMs of the two viruses, which is the most essential segment responsible for ACE2 interactions, differ only by one amino acid. Therefore, the poor binding efficiency observed between the RBD of SARS-CoV-2 and pACE2 infers that the RBD of the reported pangolin coronaviruses must bind to pACE2 fairly inefficiently. Indeed, a very recent study confirmed the case: the RBD of the pangolin coronavirus binds pACE2 ten-fold weaker than to hACE2. These observations once again refute the claim that pangolins are the probable intermediate host for SARS-CoV-2. More importantly, the latter two studies strongly suggest that these viruses might not be able to establish infections in pangolins, which adds significantly to the suspicion that the published sequences of the pangolin coronaviruses may have been fabricated and these viruses do not exist in nature.

2.4 Genetic evidence proving the fraudulent nature of the pangolin coronaviruses

Evolutionarily, within the coronavirus genome, the RBD of Spike is under the strongest positive selection as it needs to adapt for binding a new receptor whenever the virus crosses the species barrier and enters a new host. In lineage B β coronaviruses, the most essential segment for receptor recognition is the RBM, which fully determines the binding with ACE2. Strikingly, when the RBM sequence of the pangolin virus MP789 is compared to that of SARS-CoV-2, no positive selection is observed (Figure 7A). Instead, the analysis revealed very strong purifying selection with 24 syn mutations and only one non-syn mutation.

In contrast, when two related bat coronaviruses, BM48-31 and BtKY72, are compared in a similar manner, strong positive selection is observed as expected (Figure 7B). Here, while there are 25 syn mutations, which is comparable to that between MP789 and SARS-CoV-2, the number of non-syn mutations is 30 (Figure 7B). Evidently, the species difference between pangolin and human is greater than that between the hosts of BM48-31 and BtKY72, which are two different species of bats. Therefore, greater positive selection should be expected between MP789 and SARS-CoV-2 than that between BM48-31 and BtKY72. The strong purifying selection observed between MP789 and SARS-CoV-2 is, therefore, contradictory to the principles of natural evolution.

We further looked at the syn and non-syn mutations for the RBM in coronaviruses infecting the same species. Here, we compared the closely related coronaviruses ZC45 and ZXC21, which infect the same species of bats, on their RBM segments (Figure 7C). Here, twelve synonymous mutations and three nonsynonymous mutations are observed, yielding a syn/non-syn ratio of 4:1. Such a value likely represents the approximate upper limit for the purifying selection in the RBM that such coronaviruses could possibly experience (Table 3). In addition, no purifying selection is observed in the RBM for the randomly selected twenty SARS-CoV-2 sequences (Figure 5, codon range 437-507).

Therefore, the extremely high syn/non-syn ratio (24:1) observed between MP789 RBM and
SARSCoV-2 RBM indicates that at least one of the two viruses is artificial.

We believe that, to falsify the natural existence of the unique RBD/RBM of SARS-CoV-2, the amino acid sequence of the pangolin coronavirus RBD/RBM had been fabricated to closely resemble that of SARS-CoV-2. At the same time, the expert(s) carrying out this operation also wanted to create an appropriate level of divergence between the pangolin virus and SARS-CoV-2 at the nucleotide level and thereby introduced a significant amount of syn mutations in the RBM. The abnormality revealed in Figure 7A and Table 3 likely resulted from these fraudulent operations.

Similar syn/non-syn analyses on the overall spike further revealed the fraudulent nature of these novel pangolin coronaviruses. Here we compared two representative pangolin coronaviruses MP789 (a Guangdong isolate) and P4L (a Guangxi isolate) as genomic sequences within each group of isolates share very high sequence identities. As shown in Figure 8A, similar to the abnormal pattern observed between RaTG13 and SARS-CoV-2 (Figure 4A right), syn and non-syn curves exhibit drastically different trajectories and the non-syn curve abruptly flattens in the S2 half of the sequence.

For comparison, we also analyzed the spike genes of two SARS-like bat coronaviruses, BM48-31 and BtKY72. The two pangolin coronaviruses, MP789 and P4L, are 85.2% identical on the overall genome, while bat coronaviruses BM48-31 and BtKY72 are 82.4% identical. The comparison here is therefore appropriate. Analysis of the two bat viruses show that the two curves grow naturally in a relatively concerted manner with no excessive flattening of the red curve observed (Figure 8B).

Counting the number of syn and non-syn mutations in each pair of comparisons further illustrated the unnatural characteristics associated with the pangolin coronaviruses (Table 4). While the S2 protein is not expected to be more conserved than Orf1b, the syn/non-syn ratio for S2 observed in the comparison between MP789 and P4L is abnormally high (207 syn mutations and 9 non-syn mutations; syn/non-syn = 23:1), which is far exceeding what is observed for Orf1b (7.6:1).

As the two bat coronaviruses here were discovered in nature independently by research groups outside of China, the features displayed in Figure 8B likely represent the approximate evolutionary trait of two coronaviruses at this level of overall divergence. According to the logic described earlier, the great contrast between Figure 8A and 8B and the abnormal syn/non-syn ratio of 23:1 (Table 4) further prove that, between MP789 and P4L, at least one is artificial, although we believe both groups of pangolin coronaviruses represented by MP789 and P4L, respectively, are non-natural and fabricated.

2.5. Summary and discussion

A single source of samples was used for all studies (some spuriously independent7) reporting novel pangolin coronaviruses. The formats of sequencing reads were manipulated with a clear intention to hide the fact that the same dataset was used in different studies. The raw sequencing data is missing for certain critical pieces, poor in quality, and suspicious in terms of the amounts and types of contaminations present.

The RBD encoded by the reported sequence of pangolin coronaviruses could not bind pACE2 efficiently.

As revealed by syn/non-syn analyses, sequences of the RBM and S2 regions of these pangolin coronaviruses exhibit features that are inconsistent with natural evolution. Finally, no coronavirus was detected in a large, decade-long surveillance study of Malayan pangolins. These observations and evidence converge to prove that these recently reported pangolin coronaviruses do not exist in nature and their sequences must have been fabricated.

It is noteworthy that the abnormal syn/non-syn feature revealed for S2 in the comparison between MB789 and P4L (Figure 8A) resembles greatly that exhibited by the comparison between RaTG13 and SARS-CoV-2 (Figure 4A right). Judging based on this reoccurring pattern, we believe that the sequence fabrications in both cases (RaTG13 and pangolin coronaviruses) were most likely carried out by the same person or group, whose misconception of the spike gene evolution persisted in multiple such practices and resulted in the unnatural look of the syn/non-syn curves and numbers (Figure 4, Table 1, Figure 8, and Table 4).

3. Evidence revealing the fraudulent nature of the novel bat coronavirus RmYN02

While the publications of the fabricated pangolin coronaviruses might have seemingly fulfilled the scientific quests for an intermediate host for the zoonosis of SARS-CoV-2 as well as for an evolutionary origin of its RBD, it had remained suspicious and unexplainable how SARS-CoV-2 could have acquired the furin-cleavage site (-PRRAR/VS-) at the S1/2 junction through natural evolution. It is evident that, although furin-cleavage site has been found in certain other lineages of coronaviruses at the S1/2 junction, lineage B β coronaviruses clearly lack the ability to develop this motif at this location naturally.

In early June, another novel bat coronavirus, RmYN02, was reported9, which shares a 93.3% sequence identity with SARS-CoV-2 and appears to be the second closest bat coronavirus to SARS-CoV-2 (the closest is allegedly RaTG13). This finding adds yet another member to the rapidly growing sub-lineage of SARS-CoV-2-like coronaviruses (Figure 9), which has been completely vacant and practically nonexistent prior to the current pandemic. In addition, importantly, RmYN02 carries a unique sequence -PAA at the S1/S2 junction, which remotely resembles the inserted -PRRA- sequence at the same location in the SARS-CoV-2 Spike. Despite the fact that -PAA- in RmYN02 only partially resembles the -PRRA insertion in SARS-CoV-2 and does not appear to be an actual insertion if properly aligned, the authors nonetheless claimed that the natural occurrence of -PAA- in RmYN02 proves that the -PRRA- sequence could very likely be acquired and “inserted” into the same location in SARS-CoV-2 genome through natural evolution.

The fact that a poor alignment was used to make a disproportional, strong argument for an evolutionary origin of the furin-cleavage site, which appeared to be the last missing piece of the puzzle, is suspicious.

Furthermore, despite the significance of the spike sequence of RmYN02 in supporting the central conclusion of the publication, the raw sequencing reads for spike has not been made available although the authors stated otherwise in the article. This is yet another repeat of the pattern that has been exhibited in the reporting of both RaTG13 and pangolin coronaviruses, where the genomic sequence would be published first and the raw sequencing reads would not be made available months afterwards.

Given that the CCP-controlled laboratories have repeatedly engaged in fabrication of coronaviruses to feed the missing pieces for the puzzle, the above suspicion opens up the possibility that the RmYN02 virus could have been fabricated as well. Judging from the fact that its sequence identity to SARS-CoV-2 (93.3%) is lower than that between RaTG13 and SARS-CoV-2 (96.2%), we suspected that the sequence of RmYN02 might have been fabricated by modifying the sequence of RaTG13. Such an approach could easily ensure that the evolutionary distance between RmYN02 and SARS-CoV-2 is greater than that between RaTG13 and SARS-CoV-2. It also ensures that RmYN02 and RaTG13 would appear to be evolutionarily close, consistent with the claim that they both infect bats although of different species.

We therefore compared the spike genes of RmYN02 and RaTG13 on the quantity and distribution of syn and non-syn mutations. The severe divergence at the S1 portion between the two viral sequences did not allow the S1 sequences to be properly codon-aligned. Therefore, only the S2 half was analyzed (Figure 10). For the beginning 200 codons of S2, both types of mutations accumulate steadily and gradually.

However, for the final 378 codons, once again, the non-syn curve flattens and the concerted growth of the two curves has disappeared. In this region, there are 57 syn mutations and only one non-syn mutation. The syn/non-syn ratio of 57:1 for a region as wide as 378 codons (1,344 nucleotides) is severely inconsistent with what is observed naturally (Figure 4A left and Figure 8B).

Logically, between RaTG13 and RmYN02, at least one must be artificial. Here, however, we are convinced that both viruses are artificial. As shown in part 1, the sequence of RaTG13 must have been fabricated. Therefore, the fact that the last 378 codons of RmYN02’s S2 are identical, with the exception of one, to that of RaTG13 proves that the RmYN02 sequence must be artificial as well. This also proves our earlier suspicion that the RaTG13 sequence should have been used as the template for the fabrication of the RmYN02 sequence. RaTG13 was published in late January, while RmYN02 was published in early June (manuscript submitted in April). Therefore, enough time is in between for the sequence fabrication to be carried out.

While introducing nucleotide changes to create the apparent divergence between the two viruses, the expert(s) may have overly restricted amino acid changes in this part of Spike. Again, the abrupt change of trajectory of the non-syn curve and its excessive flattening later in the sequence likely reflect their overestimation of the purifying selection pressure on S2. The fact that this abnormal pattern has been observed in all three cases (Figure 4A right, 8A, and 10) reiterates the point raised in section 2.5 that all sequence fabrications may have been carried out by the same person or group.

4. Final discussion and remarks

4.1 All fabricated coronaviruses share a 100% amino acid sequence identity on the E protein with ZC45 and ZXC21


Evidence herein clearly indicates that the novel coronaviruses recently published by the CCP controlled laboratories are all fraudulent and do not exist in nature. One final proof of this conclusion is the fact that all of these viruses share a 100% amino acid sequence identity on the E protein with bat coronaviruses ZC45 and ZXC21, which, as revealed in our earlier report1, should be the template/backbone used for the creation of SARS-CoV-2 (Figure 11). Despite its conserved function in the viral replication cycle, the E protein is tolerant and permissive of amino acid mutations. It is therefore impossible for the amino acid sequence of the E protein to remain unchanged when the virus has allegedly crossed species barrier multiple times (between different bat species, from bats to pangolins, and from pangolins to humans). The 100% identity observed here, therefore, further proves that the sequences of these recently published novel coronaviruses have been fabricated.

A main goal of these fabrications was to obscure the connection between SARS-CoV-2 and ZC45/ZXC21. Therefore, from their perspective, the fabricated viruses should resemble SARS-CoV-2 more than ZC45 and ZXC21 do. Because ZC45 and ZXC21 already share a 100% identity with SARSCoV-2 on the E protein, the fabricated viruses therefore were made to adopt this sequence completely as well.

4.2 Important implications of this large-scale, organized scientific fraud

If SARS-CoV-2 is of a natural origin, no fabrications would be needed to suggest so. The current report, therefore, corroborates our earlier report and further proves that SARS-CoV-2 is a laboratory product.

As revealed, the creation of SARS-CoV-2 is convenient by following established concepts and techniques, some of which (for example, restriction enzyme digestion) are considered classic and yet still preferred widely including by experts of the field. A key component of the creation, the template virus ZC45/ZXC21, is owned by military research laboratories.

Importantly, as revealed here, multiple research laboratories and institutions have engaged in the fabrication and cover-up. It is clear that this was an operation orchestrated by the CCP government.

In addition, raw sequencing reads for RaTG13, which were integral parts of the fabrication, were obtained in 2017 and 2018. Furthermore, manuscript reporting the falsified coronavirus infections of Malayan pangolins was submitted for publication in September 2019. Evidently, the cover-up had been planned and initiated before the COVID-19 outbreak. Therefore, the unleashing of the virus must be a planned execution rather than an accident.

4.3 SARS-CoV-2 is an Unrestricted Bioweapon

Although it is not easy for the public to accept SARS-CoV-2 as a bioweapon due to its relatively low lethality, this virus indeed meets the criteria of a bioweapon as described by Dr. Ruifu Yang. Aside from his appointment in the AMMS, Dr. Yang is also a key member of China’s National and Military Bioterrorism Response Consultant Group and had participated in the investigation of the Iraqi bioweapon program as a member of the United Nations Special Commission (UNSCOM) in 1998. In 2005, Dr. Yang specified the criteria for a pathogen to qualify as a bioweapon:

1. It is significantly virulent and can cause large scale casualty.

2. It is highly contagious and transmits easily, often through respiratory routes in the form of aerosols.
The most dangerous scenario would be that it allows human-to-human transmission.

3. It is relatively resistant to environmental changes, can sustain transportation, and is capable of supporting targeted release.

All of the above have been met by SARS-CoV-2: it has taken hundreds of thousands lives, led to numerous hospitalizations, and left many with sequela and various complications; it spreads easily by contact, droplets, and aerosols via respiratory routes and is capable of transmitting from human to human, the latter of which was initially covered up by the CCP government and the WHO and was first revealed by Dr. Li-Meng Yan on January 19th, 2020 on Lude Press; it is temperature-insensitive (unlike seasonal flu) and remains viable for a long period of time on many surfaces and at 4°C (e.g. the ice/water mixture).

Adding to the above properties is its high rate of asymptomatic transmission, which renders the control of SARS-CoV-2 extremely challenging. In addition, the transmissibility, morbidity, and mortality of SARS-CoV-2 also resulted in panic in the global community, disruption of social orders, and decimation of the world’s economy. The range and destructive power of SARS-CoV-2 are both unprecedented.

Clearly, SARS-CoV-2 not only meets but also surpasses the standards of a traditional bioweapon.

Therefore, it should be defined as an Unrestricted Bioweapon.

4.4 The current pandemic is an attack on humanity

The scientific evidence and records indicate that the current pandemic is not a result of accidental release of a gain-of-function product but a planned attack using an Unrestricted Bioweapon. The current pandemic therefore should be correspondingly considered as a result of Unrestricted Biowarfare.

Under such circumstances, the infected population are being used, unconsciously, as the vectors of the disease to facilitate the spread of the infection. The first victims of the attack were the Chinese people, especially those in the city of Wuhan. At the initial stage, the hidden spread in Wuhan could have also served another purpose: the final verification of the bioweapon’s functionality, an important aspect of which is the human-to-human transmission efficiency. Upon the success of this last step, targeted release of the pathogen might have been enabled.

Given the global presence of SARS-CoV-2 and the likelihood of its long-term persistence, it is appropriate to say that this attack was on the humanity as a whole and has put its fate at risk.

4.5 Actions need to be taken to combat the current pandemic and save the future of humanity

Given the CCP’s role here, it is of paramount importance that the CCP is held accountable for its actions.

In addition, the world needs to find out what other variants of SARS-CoV-2 exist in the CCP-controlled laboratories, whether or not SARS-CoV-2 or its variant(s) are still being actively released, whether or not re-infection of SARS-CoV-2 leads to worsened outcomes due to inefficient immunity and/or antibody dependent enhancement (ADE), and whether other weaponized pathogens are owned by the CCP as a result of their excessive, state-stimulated efforts in collecting novel animal pathogens and studying their potentials in zoonosis.

It is also of paramount importance that all the hidden knowledge of SARS-CoV-2 be brought out as soon as possible. As illustrated in our earlier report, although a template virus was used, the creation of SARS-CoV-2 must have involved introducing changes to the template sequence through DNA synthesis (steps 1 and 4 in part 2 of our earlier report)1. Such a practice can be safely guided by multi-sequence alignment of available SARS and SARS-like coronavirus sequences. The process of this practice has been illustrated, and both syn mutations and amino acid (non-syn) mutations at variable positions/regions would be introduced. From the perspective of the responsible scientists, these changes are necessary because, otherwise, the engineered nature of the virus and its connection to its template would be evident.

However, importantly, the introduced changes might have also altered the functions of the various viral components, which could be either by design or unintended. Nonetheless, it remains to be answered whether or how the introduced changes might be responsible for the various lasting complications that many COVID-19 patients experience and what barriers these changes might pose to the development of effective vaccines and other antiviral therapeutics. It is reasonable to believe that the responsible laboratories under the control of the CCP have been engaged in this research for a long period of time and therefore keep in possession a considerable amount of concealed knowledge of SARS-CoV-2. Some of the knowledge may provide answers to questions that need to be addressed urgently in the global combat against COVID-19. Such hidden knowledge ought to be made available to the world immediately.

What also need to be held accountable are the individuals and groups within certain organizations and institutions in the fields of public health and academic research, who knowingly and collaboratively facilitated the CCP’s misinformation campaign and misled the world. On January 18th and 19th, 2020, Dr. Li-Meng Yan, then anonymously, first revealed that SARS-CoV-2 is of a laboratory origin.

Immediately afterwards, on January 20th, Dr. Zhengli Shi submitted her manuscript to Nature and reported the first fabricated virus, RaTG13. Since then, many virus fabrications have taken place and all of them were published as peer-reviewed articles on top scientific journals. Subsequently, based on such reports, influential opinion articles promoting the natural origin theory have then been published by prominent scientists and international organizations on such and other high-profile platforms.

In contrast to the rigorous promotion of the natural origin theory, strict censorship has been placed by these and other journals on manuscripts discussing a possible laboratory origin of SARS-CoV-2. Our earlier report, which was one of such manuscripts and published as a preprint article, also faced unfounded criticisms dressed as unbiased peer reviews from two groups of scientists led by Drs. Robert Gallo and Nancy Connell, respectively (our point-to-point responses are being prepared and will be published soon). As a result of this collaborative efforts, the public has been largely removed from the truth about COVID-19 and SARS-CoV-2, which has led to misjudgments, delayed actions, and greater sufferings of the global community. It is imperative to investigate the scientists, laboratories, institutions, and relevant collaborators responsible for the creation of SARS-CoV-2 and for the fabrications/cover-up.

It is also imperative to investigate the relevant individuals in the WHO, at the relevant scientific journals, in the relevant funding agencies, and in other relevant bodies, which have facilitated the creation of SARSCoV-2 and the scientific cover-up of its true origin while under full awareness of the nature of these operations. Finally, it also needs to be investigated which ones of the scientists engaged in the promotion of the natural origin theory were purely misled by the scientific fraud and which ones were colluding with the CCP government.

The time has come that the world faces the truth of COVID-19 and takes actions to save the future of humanity.

Acknowledgements

We thank Daoyu Zhang for sharing with us the observation of abnormal distribution of nonsynonymous mutations between RaTG13 Spike and SARS-CoV-2. We thank Francisco de Asis for revealing the filenames of the raw sequencing reads for RaTG13. We also thank other individuals, including anonymous scientists, for uncovering various facts associated with the origin of SARS-CoV-2.
 

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Dr. Li-Meng Yan reveals China’s fake science and the COVID-19 cover-up
WION
Washington
Oct 09, 2020, 05.27 PM(IST)
Written By: Lawrence Sellin

Since the beginning of the COVID-19 pandemic, the Chinese Communist Party supported by some Western scientists and a politically-motivated media have desperately tried to convince the world that the COVID-19 virus originated as a bat beta-coronavirus which underwent a natural mutation process and was then acquired by humans after exposure to infected animals.

Undoubtedly, such subterfuge is meant to protect certain vested interests, including the potentially devastating political and economic consequences for China, global corporate and private investment in China and a negative effect on scientific collaboration and research funding of major Western research laboratories.

In her first article, “Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route,” Chinese scientist and whistleblower, Dr. Li-Meng Yan presented the biological evidence demonstrating that the COVID-19 virus was made in a laboratory.

Now, Dr. Yan has published her second scientific article “SARS-CoV-2 Is an Unrestricted Bioweapon: A Truth Revealed through Uncovering a Large-Scale, Organized Scientific Fraud,” which describes the extraordinary lengths the Chinese Communist Party has gone to cover-up the true laboratory origin of the COVID-19 virus in order to escape responsibility for the pandemic.

For months after the start of the outbreak, China flooded the scientific literature with subtle and sometimes not so subtle messages supporting its narrative that COVID-19 is a naturally-occurring disease that “jumped” from animals to humans in the Wuhan seafood market.

After endless media reports and scientific studies, the theory that the Wuhan seafood market was the source for animal–human COVID-19 transmission was totally discredited, even by the Chinese Centers for Disease Control and Prevention.

On February 3, 2020, “batwoman” Dr. Zheng-Li Shi of the Wuhan Institute of Virology published an article suggesting that COVID-19 originated in bats and a bat coronavirus named RaTG13 was shown to be 96.2% identical to the COVID-19 virus, thus supporting the naturally-occurring theory.

Since then, literally hundreds of scientific articles have used RaTG13 as a basis for investigating the natural origin of the COVID-19 pandemic, despite the fact that RaTG13 exists only on paper because no live virus or intact genome of RaTG13 have ever been isolated or recovered.
Dr. Yan and her colleagues now make multiple arguments indicating that RaTG13 is a fabricated virus.

One way to determine if a virus is related to or evolved from another virus, in this case, RaTG13 and the COVID-19 virus, is to compare the synonymous and non-synonymous mutations in the genetic code.

The DNA genetic code, which is composed of combinations of the nucleotides guanine, adenine, cytosine and thymine (G, A, C and T), determines the structure of proteins. It does so through groups of three nucleotides called codons that correspond to specific amino acids, the building blocks of proteins, and that code is redundant.

For example, the amino acid arginine can be produced by codons CGT, CGA, CTC or CGG, meaning the third nucleotide in the codon is redundant or interchangeable and will still code for arginine. Any change in the first or second nucleotide will produce a different amino acid.

So, a viral genetic code can mutate, but still produce the same amino acid or a “synonymous” outcome. A mutation in the first or second nucleotide in a codon will result in different amino acid, a “non-synonymous” outcome.

In the absence of a major natural or artificial recombinant event, viruses that are naturally related or evolve from each other, as claimed for RaTG13 and the COVID-19 virus, have roughly standard ratios comparing synonymous and non-synonymous mutations.

Dr. Yan’s data show that when the ratios of synonymous and non-synonymous mutations between a critical segment of the RaTG13 and COVID-19 viruses are compared, the result “is abnormal and a violation of the principles of natural evolution.”

The interpretation is that RaTG13 and the COVID-19 virus could not be related to each other through natural evolution and that RaTG13 is a likely fabrication.

In addition, a reconstructed RaTG13 receptor binding domain does not bind to the angiotensin converting enzyme-2 receptors in two species of horseshoe bats, implying that RaTG13 could not exist in a bat population from which it would mutate and infect humans, completely undermining the naturally-occurring theory.

Dr. Yan also questions the accuracy of China’s pangolin (scaly anteater) coronavirus data upon which dozens of scientific studies examining potential natural coronavirus recombination events are based.

In early June, another novel bat coronavirus, RmYN02, which shares a 93.3% sequence similarity to the COVID-19 virus, was identified and used to support the Communist Chinese Party’s argument that the pandemic was a natural outbreak.

In that weak attempt to buttress the naturally-occurring theory, the Chinese authors of the RmYN02 article claim that a proline-alanine-alanine (PAA) amino acid insertion represents an ancestor to the proline-arginine-arginine-alanine (PRRA) furin polybasic cleavage site found in the COVID-19 virus, but not found in any other related bat coronavirus.

The presence of the furin polybasic cleavage site is a marker for genetic manipulation and, therefore, countering that fact would be an important objective of the Chinese Communist Party's propaganda machine.

The RmYN02 hypothesis disintegrates under scrutiny because the PAA sequence is chemically neutral, not basic and it could not cleave anything.

RmYN02 does not even possess the arginine-serine (R-S) cleavage point found in the COVID-19 virus and all related coronaviruses and the published RmYH02 sequence seems to be out of alignment.

Dr. Yan’s second scientific article adds one more nail in the coffin of China’s false theory that the COVID-19 pandemic was naturally-occurring.
 

johnq

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Newspaper investigation claims China hoarded face masks in early January

If true this goes to show China knew about human-to-human transmission when denying it to the world

Before the Wuhan coronavirus (COVID-19) outbreak was declared a global pandemic, Chinese consulates in Canada and around the world asked Chinese nationals to stockpile as much personal protective equipment (PPE) as possible for hospitals in China, according to an investigation by Canada's Global News.
In an article titled "United Front groups in Canada helped Beijing stockpile coronavirus safety supplies," published on Thursday (April 30), investigative reporter Sam Cooper shared his findings with Jorge Guajardo, Mexico's former ambassador to Beijing, and Canadian lawmaker Erin O'Toole.
Guajardo claimed that China had engaged in a "surreptitious" state-level operation to secure global PPE supply at low prices and did so before the deadly virus had made its way to Western countries, in early March. He said a source in the Mexican supply chain had told him in mid-January that factories were receiving large orders to send N95 respirators to China.
According to O'Toole, China had been hoarding face masks and epidemic safety equipment since Jan. 14, back when Beijing claimed there were no cases of human-to-human transmission. However, O'Toole said the Canadian government did not respond to China's acquisition campaign despite it being well-known among military and emergency service circles.
According to Cooper, while Canada was shipping more than 14,500 kilograms of protective clothing, face masks, goggles, and gloves to China, Chinese community organizations and business groups in Canada bought and shipped at least 90,700 kg of medical supplies to China. He added the stockpiling operation was launched by The United Front Work Department (UFWD) of the Chinese Communist Party (CCP), a department in charge of managing potential opposition groups in China and important foreign missions.
Cooper pointed out that China's early suppression of accurate information about the outbreak was the main cause for it becoming a pandemic, a belief shared by international media, including the Associated Press. He said that Beijing's decision to downplay the seriousness of the coronavirus has resulted in millions of individuals infected around the world.


The Chinese government allowed the virus to spread around the world by allowing international travel while stocking up on masks and PPE for itself. All the while lying to the world through WHO that there is no human-to-human transmission. But the Chinese government knew there was human-to-human transmission because they were buying up masks and personal protective equipment to protect themselves from human-to-human transmission of the Covid-19 virus they created in a lab, they leaked out, and they allowed to spread around the world (by allowing international travel of infected people).
 

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Russia To Sell 121 Helicopters To China Amidst India's Standoff With China
The Russian Helicopters holding, part of the Rostec State Corporation, will supply more than 120 helicopters, of which 18 are combat helicopters, to China under the 2019 contracts which was stated in the report of Rostec last year. This is reported by Izvestia.



“During 2019, Russian Helicopters JSC signed contracts for the supply of the following Russian-made helicopter equipment to China: 68 Mi-171 helicopters (including the upgraded Mi-171E), 18 Mi-171Sh (military transport) helicopters, 14 helicopters Mi-171 with a VK-2500 engine, 21 Ansat helicopters," the document says.



In addition, the report notes, that JSC Russian Helicopters handed over the first eight helicopters to the Russian National Air Ambulance Service: four Ansats and four Mi-8s. By 2021, the organization plans to deliver 87 medical helicopters.



“JSC Russian Helicopters, within the framework of the MAKS-2019 aerospace show, presented for the first time the Ansat helicopter with a high comfort cabin made in the style of the Aurus brand,” the document says.



The interior design project was created by employees of JSC Russian Helicopters and the Scientific Research Automobile and Automotive Institute.

Key Acquisition: Mi-171Sh Assault Transport Helicopter



The Russian military is preparing for a significant "storm" development – as in serial production of its upgraded Mi-171Sh Storm military transport helicopter, which will be equipped with guided missiles. Production on the new model will begin in two years, state media reported.



The Mi-171Sh is the latest updated version of the Mi-17, which entered service in the Soviet Red Army in the 1970s and which saw use as an armed gunship version.



Mission And Primary Tasks



The Mi-171Sh military/transport helicopter is designed to transport personnel, cargo and equipment inside the cargo cabin or on an external sling, drop tactical air assault forces and reconnaissance and sabotage groups, destroy ground targets and carry the wounded. Additional versions of the helicopter are available: search & rescue, fire-fighting, ambulance, corporate.

Airborne Equipment And Armaments


The Mi-171Sh was specifically designed for operating in combat missions in local armed conflicts. The design incorporates a five-bladed main rotor, a tail rotor and non-retractable tricycle nose-wheel landing gear.

The glassed-in cockpit accommodates three crew and cabin houses up to 36 troops, or up to 12 casualties on stretchers. The helicopters are equipped with modern avionics and instrumental equipment, to operate in all weather conditions at any time of the day.

The armour protection provided over the crew cabin and vital units increases the combat survivability of the helicopter. The helicopter has an IR-decoy dispensing system to counter an infrared homing surface-to-air missile or air-to-air missile.

The fuel tank self-sealing covers and polyurethane foam protection avoid the possibility of fuel explosions and leakage in case of combat damage.

The Mi-171Sh is armed with a Shturm-V high-precision guided missile system. The missiles can destroy modern battle tanks protected by explosive reactive armour, fortified points and aerial targets.

The Shturm-V missile complex launches Ataka supersonic missiles equipped with a hollow-charge warhead for defeating armoured targets. The missile can destroy aerial targets with a fragmentation warhead and lightly armoured combat materiel by using a high-explosive warhead.

The Mi-171Sh is also provided with hardpoints to carry up to 80 S-8 unguided rockets and GSh-23L 23mm cannons, with an ammunition load of 500 rounds.

Key Advantages



  • operability in any geographical and climatic conditions, day and night, and low weather;
  • operability in high-altitude and hot conditions;
  • versatility (capability to effectively perform assault/transport and combat tasks during one mission sortie);
  • capability to land on unprepared sites at night and in limited adverse weather conditions;
  • heavy armour protection;
  • high target approach accuracy through the use of a satellite navigation system;
  • high safety and single-engine flight and landing capability;
  • high efficiency of loading/unloading of cargo and paratroopers through the presence of two doors on the sides of the helicopter and a powered ramp.
 

Haldilal

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The Radar station mer the Bhutanese border.
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Haldilal

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J 10's Double seater I thinks this are of the PLAN.
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Haldilal

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Ya'll Nibbiars another Called exercise.
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EnJ65eeUYAUD_K4.jpeg
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Haldilal

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Ya'll Nibbiars The Mlecchas have connected almost every border post to the grid.
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Haldilal

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Ya'll Nibbiars The JH 7 conduting bombing raids.
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Haldilal

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Ya'll Nibbiars Copy of the Eurofighter helmet? STRIKER-2 HMD's.
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