Red Reishi Extract & Covid-19

Yeah, I read that one when it came out. Then I read the Harvard professor's rebuttal of it that I linked and looked more into it.

This evidence for natural evolution was supported by data on SARS-CoV-2's backbone -- its overall molecular structure. If someone were seeking to engineer a new coronavirus as a pathogen, they would have constructed it from the backbone of a virus known to cause illness. But the scientists found that the SARS-CoV-2 backbone differed substantially from those of already known coronaviruses and mostly resembled related viruses found in bats and pangolins.

"These two features of the virus, the mutations in the RBD portion of the spike protein and its distinct backbone, rules out laboratory manipulation as a potential origin for SARS-CoV-2" said Andersen.

That's the assertions of the people in the article you linked. But think about that for a second. If you were researching viruses, and engineering new ones, would you not be trialing wild viruses in bats, too? Why would we assume that any human engineered virus has to come from the backbone of another human virus? That makes zero sense when you think about it. I'll quote a few responses from the blog I linked above.

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.

* The most recent study, covered in our article, that examines the neutral sites that are assumed to best show heritage found that pangolins are “very unlikely” to have served as a host at all. Their assertion that natural natural selection is clearly shown is raw steamy bullshit. Serial passage through ferrets fits the overall big picture far better than this pangolin crap.

______________________________

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.

* WAIT WAIT WAIT!! You mean exactly like a bunch of ferrets, which have the same ACE2 receptor as humans, all jammed into a bunch of cages together and then infected over and over again in a lab?! That’s crazy talk!! Other than the fact it was exactly the process used to make the Bird Flu into something that “could make the 1918 pandemic look like a pesky cold.”

_______________________________

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 it1,2.

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.

* Sure this would be plausible… other than the fact that, as we cover in our report, that statistical analysis shows that this thing didn’t hit humans until November of 2019, which this article agrees with. But zoonotic jumps only occur after a genomic trial-and-error process where the virus jumps to one host, spreads to a few new hosts, and then fizzles out. There is absolutely no evidence anywhere of this occurring. Every single data points to this thing hitting humans in November and being immediately adapted and dangerous. There is no trace whatsoever of it creating small clusters of infections and dying out – stating there could have been doesn’t mean it’s been seen. It hasn’t. And as our report covers, this would require sustained interaction with the intermediate host – how does that happen in the middle of a massive modern urban metropolis the size of NYC? And where is this intermediate host anyways? If an intermediate host isn’t needed, is it some magical sleep-flying bat that decided not to hibernate and fight crime in Wuhan when it’s buddies were all hibernating, creating the sustained interactions with humans as it fought for Justice? Because that’s about as plausible as what’s being proposed here.

_______________________________

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.

* Again, analysis of the neutral sites shows that pangolins were almost certainly not in play.

_______________________________

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

* This means nothing. There is no open-source shared database of viruses. No one has any idea what viruses are in China’s BSL-4 lab, where they’ve been collecting these viruses for years. As mentioned, one of our persons-of-interest was the very first person to isolate a coronavirus from a bat that uses the ACE2 receptor. He also worked at UNC in Baric’s lab making the hyper-virulent bat coronavirus in 2015.

I won't quote his whole rant, but that is what initially got me researching this more. Then when I read more into the specifics of what we know about the genome, and how well this thing binds to ACE2, I started to kind of get onboard with this guy's position.