SARS-CoV-2 has a very unusual feature: it is surprisingly good at infecting a particular type of cell that has what is known as an angiotensin-converting enzyme 2 receptor. Some other animals have ACE2 receptors, but SARS-CoV-2 works much better in human or human-like ACE2 receptors. The significance of this cannot be overemphasized.
SARS-CoV-2 needs four things to happen to infect a human. It must enter the body and it must attach to certain cells. It must be cleaved at precisely the correct spot by the victim’s cells. The remaining genetic piece must then enter and infect the cell. Every one of these four steps has a low probability of occurring by chance. The probability of all four of these unlikely events developing randomly through mutations is, therefore, very low.
Could SARS-CoV-2 have acquired its clever attributes from another coronavirus of the same family? Are there coronaviruses that exploit human-like ACE2 receptors? For this, we need to discuss the furin cleavage site, which is where the ACE2 receptor precisely cuts SARS-CoV-2, as described in step 3 above.
This is from Charles L. Hooper and David R. Henderson, “The Origin of SARS-CoV-2,” AIER, June 18, 2021.
Location, Location, Location
If camels infected humans in the Middle East, we wouldn’t expect to see the first cluster of cases in, say, Honolulu. Early cases typically happen where the virus first became contagious. And even if people travel, they are likely to become sick or infect others en route, leaving a trail of evidence.
There are nine Metro lines and 40 hospitals in Wuhan and yet all the patients treated for Covid-19 between 1 December 2019 and early January 2020 were cared for in hospitals close to the Metro Line 2 commuter line, connecting Wuhan and WIV. That’s highly unlikely by random chance alone.
Charley did all the research for this and almost all the writing. I edited it but he very generously gave me co-authorship.
Read the whole thing.
Source – www.econlib.org