One of the most resilient conspiracy theories that has emerged during our forced isolation in the midst of the SARS-CoV-2 pandemic is that it is a man-made virus. Some officials of the Trump administration are squarely laying the blame of this pandemic on a bio-engineering product let loose from the Wuhan Institute of Virology, a few kilometers away from that infamous “wet market” in the city center. They claim that lax security measures at the institute provoked the fatal accident.
The SARS-CoV-2 virus is the seventh coronavirus that infected humans recently; SARS-C0V, MERS-CoV and SARS-CoV-2 can produce grave clinical symptoms while HKU1, NL63, OC43 and 229E produce much milder ones. The viral load of bats has been studied for many years, but it is woefully under-sampled at present. Kristian G. Andersen, Andrew Rambaut, W.Ian Lipkin and Edward C.Holmes studied the genomic material of the virus to determine if it was actually man-made.
Based on structural studies and biochemical experiments, the researchers found that:
- The virus seems to be optimized for binding to the human receptor ACE2
- The spike protein of the virus has a functional (furin) cleavage site at the S1-S2 boundary, which predicted an acquisition of three O-linked glycans.
Viruses bind to a host cell in order to invade them for replication of their genetic material through their receptor-binding domain (RBD) The researchers found that SARS-CoV-2 has an RBD that binds with optimal affinity to ACE2 from human beings, ferrets and cats. However, analysis made with computer programs showed that the RBD sequence is not the ideal one for optimal receptor binding. Therefore they concluded that it was the result of a natural selection process of trial and error and not the calculated result of some perfidious manipulation by wacky warmongers.
The second characteristic of this virus is that it has a polybasic cleavage site (RRAR) at the junction of two subunits of the spike, S1 and S2; this enables the cleavage of proteases like furin, which has a critical role in the high infectivity and host range. These cleavage sites have not been observed in other coronaviruses, but they appear in other kind of betacoroanviruses infecting humans, which indicates they will be found in other species. Some experiments showed that the insertion of a furin at the cleavage site enhance the anchoring to the host cell without affecting viral entry. The function of the predicted 0-linked glycans has not been determined but it could represent a “mucin-like domain” to mask the virus spikes, thus fooling our defenses. This highly favorable medium had not been previously discovered by scientists.
Moreover, these scientists affirmed that if there had been a willful genetic manipulation, one of the previously existing reverse-genetic systems would have been used as a viral scaffolding to construct a biological weapon worthy of the Devil. The authors propose two alternative scenarios of the origin of the SARS-CoV-2:
- Natural selection in an animal host before the zoonotic jump into humans.
- Natural selection in a human being after the zoonotic jump had happened.
Considering that the SARS-CoV-2 is very similar to other bat SARS-COV-like coronaviruses, it is possible that an animal source was present in that Wuhan market; the illegally imported Malayan pangolins harbor coronaviruses similar to SARS-CoV-2. But neither the bat nor pangolin coronaviruses have the polybasic cleavage sites, which questions their possible progenitor role for this virus. They said: “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 a natural selection to proceed efficiently) and an ACE2-encoding gene that is similar of the human ortholog.”
The genetic study of all the different variants of the SARS-CoV-2 indicate that there was a common ancestor that made the jump from an animal to a human being—the definition of a zoonosis or a human disease of animal origin. The RBD found in the virus infecting the pangolins is similar to the human variant; the insertion of the polybasic cleavage might have happened during the human-to-human transmission. Computer analyses point to an emergence of the virus in late November 2019, which implies that there was a silent transmission in humans between the zoonotic jump and the insertion of the second feature, the polybasic cleavage site.
Based on these findings, the researchers concluded that there is no scientific basis to determine that this lethal agent was the product of bioengineering in a military lab.
Imbued with Humanistic values, we cannot fathom that it could be a human product.
Sadly, the amazing capacity of human beings to harm other species, including their own kind, has been an historically tragic box of nasty surprises.
The troubling image of Dr. Strangelove (played by the great Peter Sellers) jumps into our mind…
Stay distant. Stay safe. Stay beautiful.
What do you think? Please tell us.
Don’t leave me alone.