Maybe you shouldn’t blindly believe everything you read? Even if the source has a pretty solid reputation?

Nature magazine has censored over 1,000 articles at the request of the Chinese government over the past several years. And it seems pretty clear that their recent article, “The proximal origin of SARS-CoV-2” is just one more example of their influence.

China bought off the head of Harvard’s chemistry department, you don’t think they could buy off run-of-the-mill research scientists scrambling for tenure and funding and publication? It’s absolutely horrific that so many scientists and researchers are taking part in what’s really clearly a disinformation campaign orchestrated by the Chinese Communist Party, and willfully spreading a smokescreen about something that’s already killed thousands and is projected to kill millions more across the planet.

And while the mainstream corporate media mindlessly regurgitates claims from the Chinese government that are falsifiable with the simplest of google searches, allowing the public to be lulled into a false sense of security and complacency, and Reddit rapidly censors and moderates anything that might indicate that this virus leaked from a Chinese lab and so the Chinese government is to blame for this pandemic  – sites like ZeroHedge, that have been at the forefront of keeping the lines of investigation open, have been banished from Twitter and marginalized.

Below is a takedown of that article, and the good news is a much more nuanced and honest look at the origins of COVID-19, the Wuhan Strain of coronavirus is just a click away.

Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

Given the level of genetic variation in the spike, it is likely that SARS-CoV-2-like viruses with partial or full polybasic cleavage sites will be discovered in other species.

The functional consequence of the polybasic cleavage site in SARS-CoV-2 is unknown, and it will be important to determine its impact on transmissibility and pathogenesis in animal models. Experiments with SARS-CoV have shown that insertion of a furin cleavage site at the S1–S2 junction enhances cell–cell fusion without affecting viral entry14.

The acquisition of polybasic cleavage sites by HA has also been observed after repeated passage in cell culture or through animals17.

It is improbable that SARS-CoV-2 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus. As noted above, the RBD of SARS-CoV-2 is optimized for binding to human ACE2 with an efficient solution different from those previously predicted7,11.

Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used19

Instead, we propose two scenarios that can plausibly explain the origin of SARS-CoV-2: (i) natural selection in an animal host before zoonotic transfer; and (ii) natural selection in humans following zoonotic transfer.

Malayan pangolins (Manis javanica) illegally imported into Guangdong province contain coronaviruses similar to SARS-CoV-221. Although the RaTG13 bat virus remains the closest to SARS-CoV-2 across the genome1, some pangolin coronaviruses exhibit strong similarity to SARS-CoV-2 in the RBD, including all six key RBD residues21 (Fig. 1). This clearly shows that the SARS-CoV-2 spike protein optimized for binding to human-like ACE2 is the result of natural selection.

For a precursor virus to acquire both the polybasic cleavage site and mutations in the spike protein suitable for binding to human ACE2, an animal host would probably have to have a high population density (to allow natural selection to proceed efficiently) and an ACE2-encoding gene that is similar to the human ortholog.

It is possible that a progenitor of SARS-CoV-2 jumped into humans, acquiring the genomic features described above through adaptation during undetected human-to-human transmission. Once acquired, these adaptations would enable the pandemic to take off and produce a sufficiently large cluster of cases to trigger the surveillance system that detected it.

Hence, this scenario presumes a period of unrecognized transmission in humans between the initial zoonotic event and the acquisition of the polybasic cleavage site. Sufficient opportunity could have arisen if there had been many prior zoonotic events that produced short chains of human-to-human transmission over an extended period.

The presence in pangolins of an RBD very similar to that of SARS-CoV-2 means that we can infer this was also probably in the virus that jumped to humans.

Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of a progenitor virus with very high genetic similarity, which has not been described

Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described.

Retrospective serological studies could also be informative, and a few such studies have been conducted showing low-level exposures to SARS-CoV-like coronaviruses in certain areas of China26. Further serological studies should be conducted to determine the extent of prior human exposure to SARS-CoV-2.

The finding of SARS-CoV-like coronaviruses from pangolins with nearly identical RBDs, however, provides a much stronger and more parsimonious explanation of how SARS-CoV-2 acquired these via recombination or mutation1

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