There was a time when the Covid pandemic seemed to confirm so many of our assumptions. It cast down the people we regarded as villains. It raised up those we thought were heroes. It prospered people who could shift easily to working from home even as it problematized the lives of those Trump voters living in the old economy.

Like all plagues, Covid often felt like the hand of God on earth, scourging the people for their sins against higher learning and visibly sorting the righteous from the unmasked wicked. “Respect science,” admonished our yard signs. And lo!, Covid came and forced us to do so, elevating our scientists to the highest seats of social authority, from where they banned assembly, commerce, and all the rest.



We cast blame so innocently in those days. We scolded at will. We knew who was right and we shook our heads to behold those in the wrong playing in their swimming pools and on the beach. It made perfect sense to us that Donald Trump, a politician we despised, could not grasp the situation, that he suggested people inject bleach, and that he was personally responsible for more than one super-spreading event. Reality itself punished leaders like him who refused to bow to expertise. The prestige news media even figured out a way to blame the worst death tolls on a system of organized ignorance they called “populism.”
In reaction to the fool Trump, liberalism made a cult out of the hierarchy of credentialed achievement in general But these days the consensus doesn’t consense quite as well as it used to. Now the media is filled with disturbing stories suggesting that Covid might have come — not from “populism” at all, but from a laboratory screw-up in Wuhan, China. You can feel the moral convulsions beginning as the question sets in: What if science itself is in some way culpable for all this?

viruses from bat and pangolin infected the same cell in the same organism simultaneously, a rather improbable event considering the low population density of pangolins, the dearth of CoV-infected specimens in their natural populations, and the fact that CoV RATG13 does not have significant affinity for the pangolin ACE2,(3) and therefore is unlikely to penetrate the infected pangolin cell.

Gain-of-function recombinations of coronaviruses have been ongoing in the laboratory for more than a decade.(1) As early as 2007, the group headed by Zheng-li Shi from the Wuhan Institute of Virology (WIV) created a series of “bat-man” CoV chimeric spike proteins(1,4) to enable CoVs to jump from one species to another and model “spillover effects” that could trigger a pandemic. Shi’s goal was to turn the bat CoVs into huACE2-binding molecules, that is, to design promoters of human infection.(1,3,4)

With regard to the recent history of these gain-of-function manipulations of coronaviruses, a U.S. NIH funded $3.7 million grant was approved by Trump’s COVID-19 advisor Anthony Fauci in 2015. The gain-of-function research was outsourced to the WIV, which remains at the center of scrutiny with regard to the COVID-19 pandemic.(5)

An indicator that the NIH-funded research had gone too far arose when the tinkered CoV-RaTG13 became endowed at the spike protein with a “detonator”, that is, a cleavage site recognized and activated by the host-cell enzyme furin (Figure 1).(6) This site has not been identified in other CoVs from the same lineage. The way this cleavage site is incorporated attests to the artificial origin of SARS-CoV-2. The furin-associated cleavage site was created by incorporation of the 12-nucleotide insert TCCTCGGCGGGC coding for the PRRA amino acid sequence at the S1/S2 junction in the spike monomer. Strikingly, the two adjacent arginines are coded by two consecutive CGG codons. Only about 5% of arginines in SARS-CoV-2 or RaTG13 are coded by CGG.(3) This implies that the CGGCGG in the inset would have an estimated 0.25% probability to “naturally” occur as an encoder of the RR motif. Other suspicious aspects pertain to the way in which the encoding cassette was inserted to create the cleavage site. The insertion causes a split in the original codon for serine (TCA) in RaTG13,(3) so the TC portion becomes now part of a new codon for serine (TCT), while the terminal adenosine (A) becomes part of a codon for alanine (GCA), yielding the following sequence: TC[TCCTCGGCGGGC]A. This is very odd, clearly pointing to an artificial origin.

Figure 1

Figure 1. Two gain-of-function modifications of bat CoV RaTG13 promoting transmission to humans.