Guest post by Col. Lawrence Sellin (Ret.)
Despite exhaustive international research efforts, a natural source for the COVID-19 virus, whether directly from bats to humans or through an intermediate animal host, has not been identified.
Since the onset of the pandemic, the Chinese Communist Party, together with the support or acquiescence of the majority of the Western scientific community, have insisted that the COVID-19 virus was a naturally-occurring, animal-to-human transmission.
However, there is still no convincing scientific evidence that the COVID-19 virus originated from any natural source, whereas the evidence for a laboratory origin is extensive and increasing.
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In the end, it is simply a matter of whether you want to believe a narrative shaped by those with vested interests or you want to believe the facts.
The genetic engineering and related laboratory techniques to manufacture a virus like COVID-19 have existed for more than 20 years.
Over time, those techniques have only become more sophisticated, such that it is now impossible to distinguish between a natural and a man-made virus.
The COVID-19 virus has a number of unique structural features that cannot be explained as products of a natural evolutionary process.
Those anomalies primarily affect the COVID-19 virus’ extraordinarily high infectivity rate of +100,000,000 compared to, for example, the 8,096 in the first 2002-2004 SARS pandemic.
That increase in infectivity is directly related to the enhanced ability of the COVID-19 virus to bind to and enter human cells, both of which can be achieved by laboratory manipulation.
The COVID-19 virus binds to human cells 10-20 times better than the 2002-2004 SARS virus (1,2).
From the beginning, the COVID-19 virus appeared to be well-adapted (3,4) even pre-adapted (5) for binding to human cells.
The COVID-19 virus did not undergo the same mutation and adaptation to humans over time as did the 2002-2004 SARS virus, but was already, from the beginning, resembling late-stage SARS infections, suggesting pre-adaptation (5).
Such pre-adaption for human infection can be accomplished in the laboratory by repeatedly exposing coronaviruses to genetically-engineered mice that have the human receptor, a process known as serial passage.
Since 2007, Chinese scientists have used humanized mouse models to experiment with coronaviruses starting with the 2002-2004 SARS virus (6).
The second unique feature of the COVID-19 virus affecting infectivity is the presence of a furin polybasic cleavage site, a structure that facilitates membrane fusion between the virus and human cells.
The furin polybasic cleavage site is essential for human infection (7) and is a structure known by Chinese scientists to also enhance pathogenicity (8), but a structure not found in any bat coronaviruses closely related to the COVID-19 virus (7).
The unique COVID-19 virus polybasic cleavage site insertion is a short sequence of the amino acids, proline-arginine-arginine-alanine or “PRRA.”
The combination of genomic nucleotides that codes for the two joint arginines (RR), a double cytosine-guanine-guanine or CGG-CGG sequence is extremely rare, being the only instance of it in the entire COVID-19 viral genome (9).
In addition, the presence of the structurally rigid amino acid proline in the PRRA insert is also unusual. It causes the furin polybasic cleavage site to protrude from the surrounding structure making it more accessible to the enzymes on the human cell surface, thereby facilitating virus entry.
Coupled with the surrounding structure, insertion of a rigid proline could increase antigenicity, making vaccine development easier, but such a feature is not advantageous to a virus undergoing natural evolution.
In 2004, at the end of the first SARS pandemic, a U.S. patent, entitled “Inserton of Furin Protease Cleavage Sites in Membrane Proteins and Uses Thereof” was filed describing how furin polybasic cleavage sites could be artificially inserted into viruses.
During the 17 years since that patent was filed, it has only been cited 23 times, one of which was by Chinese People’s Liberation Army-trained scientists Shibo Jiang and Shuwen Liu, who, in 2013, were artificially inserting furin polybasic cleavage sites in experiments involving viruses (10).
Shibo Jiang, Shuwen Liu and their Chinese colleagues, many of whom have connections to the People’s Liberation Army and the Wuhan Institute of Virology, would become major players in the coronavirus research leading up to the COVID-19 pandemic.
I have only provided the most obvious anomalies, but there are far more examples indicating that the COVID-19 virus was created in a laboratory.
After the first SARS pandemic, scientists attempted to predict the emergence of future outbreaks by experimenting with the structural features of bat coronaviruses, including genetic engineering.
It was hoped that such experiments could provide insight about how animal to human transmission evolves and, thus, be better prepared to prevent a pandemic by having the platforms in place for rapid diagnosis, treatment and vaccine development.
Instead, the laboratory manipulation of coronaviruses actually resulted in an artificial acceleration of evolution and the emergence of an entirely unique and more infectious pathogen, whose development can be documented in the chronology of scientific articles published between the first SARS pandemic and the onset of COVID-19.
Based on the available scientific evidence, the COVID-19 virus was the product of “gain of function” research, not a natural transmission from an animal host to humans.
Gain of function research is defined as when a naturally-occurring virus is genetically or otherwise manipulated to make it either more contagious, more lethal, or both.
There are only two reasons for conducting gain of function research, (a) to understand the structural features and actions of a virus to create a vaccine in anticipation of a potential disease outbreak or (b) to create a biological weapon, or both.
It is most likely that China was conducting parallel development of a unique genetically-engineered coronavirus pathogen and a vaccine to treat it.
One such approach has been the development of live-attenuated vaccines like those used for the childhood diseases measles, mumps, rubella and chickenpox, in which a weakened or “attenuated” form of the virus that causes the disease is manufactured.
Because live-attenuated vaccines are so similar to the natural infection that they help prevent, a strong and long-lasting, even life-time immune response can be produced.
In a 2018 scientific article (11), Dr. Ralph Baric of the University of North Carolina, a long-time collaborator with the Wuhan Institute of Virology, offered a strategy for the development of a broad-spectrum, live-attenuated vaccine for coronaviruses.
Baric also identified the inherent danger of live-attenuated virus vaccines, that they have been shown to revert back to their original pathogenic state after administration to a recipient.
China’s People’s Liberation Army acknowledged the advantages of live-attenuated COVID-19 vaccines for rapid development and the induction of high immune responses (12).
In two of my articles (13,14), I cited evidence supporting the argument that the COVID-19 virus originated in connection with China’s vaccine development program, in which, either the virus itself leaked or a live-attenuated virus reverted to its deadly form after human vaccination and escaped from laboratory containment or another controlled facility.
Lawrence Sellin, Ph.D. is retired from an international career in business and medical research with 29 years of service in the US Army Reserve and a veteran of Afghanistan and Iraq. His email is [email protected]
Sources Noted Above:
(1) Khatri I, Staal FJT, van Dongen JJM. Blocking of the High-Affinity Interaction-Synapse Between SARS-CoV-2 Spike and Human ACE2 Proteins Likely Requires Multiple High-Affinity Antibodies: An Immune Perspective. Front Immunol. 2020;11(September):1-9. doi:10.3389/fimmu.2020.570018
(2) D’Amico F, Baumgart DC, Danese S, Peyrin-Biroulet L. Diarrhea During COVID-19 Infection: Pathogenesis, Epidemiology, Prevention, and Management. Clin Gastroenterol Hepatol. 2020 Jul;18(8):1663-1672. doi: 10.1016/j.cgh.2020.04.001. Epub 2020 Apr 8. PMID: 32278065; PMCID: PMC7141637.
(3) Sakshi Piplani, Puneet Kumar Singh, David A. Winkler, Nikolai Petrovsky. In silico comparison of spike protein-ACE2 binding affinities across species; significance for the possible origin of the SARS-CoV-2 virus. arXiv:2005.06199
(4) Delgado Blanco J, Hernandez-Alias X, Cianferoni D, Serrano L. In silico mutagenesis of human ACE2 with S protein and translational efficiency explain SARS-CoV-2 infectivity in different species. PLOS Comput Biol. 2020;16(12):e1008450. doi:10.1371/journal.pcbi.1008450
(5) Zhan SH, Deverman B, Chan YA. SARS-CoV-2 is well adapted for humans. What does this mean for re-emergence? Published online 2020:1-28. doi:10.1101/2020.05.01.073262
(6) Yang, Xiu-hong; Deng, Wei; Tong, Zan; Liu, Yan-xia; Zhang, Lian-feng; Zhu, Hua; Gao, Hong; Huang, Lan; Liu, Ya-li; Ma, Chun-mei; Xu, Yan-feng; Ding, Ming-xiao; Deng, Hong-kui; Qin, Chuan. Mice Transgenic for Human Angiotensin-converting Enzyme 2 Provide a Model for SARS Coronavirus Infection. Comparative Medicine, Volume 57, Number 5, October 2007, pp. 450-459 (10).
(7) Markus Hoffmann, Hannah Kleine-Weber, Stefan Pöhlmann. A Multibasic Cleavage Site in the Spike Protein of SARS-CoV-2 Is Essential for Infection of Human Lung Cells. Molecular Cell, Volume 78, Issue 4 2020, Pages 779-784.
(8) Cheng J, Zhao Y, Xu G, Zhang K, Jia W, Sun Y, Zhao J, Xue J, Hu Y, Zhang G. The S2 Subunit of QX-type Infectious Bronchitis Coronavirus Spike Protein Is an Essential Determinant of Neurotropism. Viruses. 2019 Oct 22;11(10):972. doi: 10.3390/v11100972.
(9) Segreto R, Deigin Y. The genetic structure of SARS-CoV-2 does not rule out a laboratory origin: SARS-COV-2 chimeric structure and furin cleavage site might be the result of genetic manipulation. Bioessays. 2021 Mar;43(3):e2000240. doi: 10.1002/bies.202000240
(10) Zhou Y, Wang J, Zhou I, Lou H, Li C-Z, et al. (2013) Simultaneous Expression of Displayed and Secreted Antibodies for Antibody Screen. PLoS ONE 8(11):e80005. doi:10.1371/journal.pone.0080005
(11) Menachery VD, Gralinski LE, Mitchell HD, Deinnon KH, III, Leist SR, Yount BL, Jr, McAnarney ET, Graham RL, Waters KM, Baric RS. 2018. Combination attenuation offers strategy for live attenuated coronavirus vaccines. J Virol 92:e00710-18. https://doi.org/10.1128/JVI.00710-18.
(12) Shang, W., Yang, Y., Rao, Y. et al. The outbreak of SARS-CoV-2 pneumonia calls for viral vaccines. npj Vaccines 5, 18 (2020). https://doi.org/10.1038/s41541-020-0170-0
(13) Sellin, Lawrence. Is the COVID-19 Pandemic a Case of Vaccine Research Gone Wrong? Citizens Commission on National Security. October 1, 2020.
(14) Sellin, Lawrence. Are the Global Scientific Elite Trying to Bury the Truth About the Origin of COVID-19? Citizens Commission on National Security. October 4, 2020.
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