Before the United States and many other countries had their first COVID cases, one person was out on the full-court press to shield the Wuhan Institute of Virology and the Chinese government from suspicions that the virus was engineered: Peter Daszak. Daszak, the President of EcoHealth Alliance, a New York-based non-profit that funds viral research around the globe, has had his fingers in almost all of the pies dealing with COVID-19, including “organizing” virologists to sign on to the a lette in “Lancet” stating conclusively that the virus originated naturally, serving on Lancet’s COVID-19 Origins Committee and on the World Health Organization’s team that investigated the origins; in addition, he played a significant role in funding gain-of-function research at the Wuhan Institute of Virology.
That original letter, published by The Lancet in February 2020, vehemently denied any suggestion that the SARS-CoV-2 virus may have originated at the Wuhan Institute of Virology but failed to mention Daszak’s massive conflict of interest: Daszak’s EcoHealth Alliance funded that very research and he had performed research of his own at the Chinese lab. Daszak had communications with Anthony Fauci in the early days of the pandemic, praising him for “debunking” the lab-leak theory publicly, an act that likely provided cover for Daszak’s dirty deeds.
While here at RedState we have long been pointing out the sins of Daszak, the media and science community is only now beginning to recognize the significant likelihood that this virus originated at the Wuhan Institute of Virology. Just this week, a team of 16 international scientists and epidemiologists published a letter in The Lancet condemning the cover-up and requesting a more open debate about the origins of SARS-CoV-2.
The letter, entitled “An appeal for an objective, open, and transparent scientific debate about the origin of SARS-CoV-2,” includes Rutgers’ Dr. Richard H. Ebright as an author, who has long speculated about the origins of COVID-19 and has suggested a more open investigation into the origins of the virus.
The letter begins:
On July 5, 2021, a Correspondence was published in The Lancet called “Science, not speculation, is essential to determine how SARS-CoV-2 reached humans”. The letter recapitulates the arguments of an earlier letter (published in February, 2020) by the same authors, which claimed overwhelming support for the hypothesis that the novel coronavirus causing the COVID-19 pandemic originated in wildlife. The authors associated any alternative view with conspiracy theories by stating: “We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin”. The statement has imparted a silencing effect on the wider scientific debate, including among science journalists. The 2021 letter did not repeat the proposition that scientists open to alternative hypotheses were conspiracy theorists, but did state: “We believe the strongest clue from new, credible, and peer-reviewed evidence in the scientific literature is that the virus evolved in nature, while suggestions of a laboratory leak source of the pandemic remain without scientifically validated evidence that directly supports it in peer-reviewed scientific journals”. In fact, this argument could literally be reversed. As will be shown below, there is no direct support for the natural origin of SARS-CoV-2, and a laboratory-related accident is plausible.
For a long time, I have been stating this very thing at RedState. The fact that we were not even allowed to consider that a virus that shows many benchmarks for genetic research could have been created in or released from a lab that was conducting that very type of research on the very type of viruses that would create a virus like SARS-CoV-2 is, in itself, unscientific. The quest for science doesn’t start by eliminating possible outcomes regardless of how unlikely the persons conducting the experiments, may feel it is.
As the letter continues, it gets more specific as to mistakes made by those denying the lab-leak theory:
There is so far no scientifically validated evidence that directly supports a natural origin. Among the references cited in the two letters by Calisher and colleagues, all but one simply show that SARS-CoV-2 is phylogenetically related to other betacoronaviruses. The fact that the causative agent of COVID-19 descends from a natural virus is widely accepted, but this does not explain how it came to infect humans. The question of the proximal origin of SARS-CoV-2—ie, the final virus and host before passage to humans—was expressly addressed in only one highly cited opinion piece, which supports the natural origin hypothesis, but suffers from a logical fallacy it opposes two hypotheses—laboratory engineering versus zoonosis—wrongly implying that there are no other possible scenarios. The article then provides arguments against the laboratory engineering hypothesis, which are not conclusive for the following reasons. First, it assumes that the optimisation of the receptor binding domain for human ACE2 requires prior knowledge of the adaptive mutations, whereas selection in cell culture or animal models would lead to the same effect. Second, the absence of traces of reverse-engineering systems does not preclude genome editing, which is performed with so-called seamless techniques. Finally, the absence of a previously known backbone is not a proof, since researchers can work for several years on viruses before publishing their full genome (this was the case for RaTG13, the closest known virus, which was collected in 2013 and published in 2020).
Based on these indirect and questionable arguments, the authors conclude in favour of a natural proximal origin. In the last part of the article, they briefly evoke selection during passage (ie, experiments aiming to test the capacity of a virus to infect cell cultures or model animals) and acknowledge the documented cases of laboratory escapes of SARS-CoV, but they dismiss this scenario, based on the argument that the strong similarity between receptor binding domains of SARS-CoV-2 and pangolins provides a more parsimonious explanation of the specific mutations. However, the pangolin hypothesis has since been abandoned, so the whole reasoning should be re-evaluated.
Among the most interesting things said above is the direct reference to RaTG13, a virus found in the Yunnan Province in China in 2013, that had been taken back to the Wuhan Institute of Virology shortly after it was discovered. I have long hypothesized that RaTG13, another SARS-like Coronavirus, could have likely served as the backbone for SARS-CoV-2, as it shares 96.2% of its genomic code with that virus. While the scientists here don’t explicitly state that RaTG13 was the backbone for SARS-CoV-2, I find it interesting that they reference this virus directly while talking about identifying a potential backbone they could have used to synthesize the virus.
The letter continues:
Although considerable evidence supports the natural origins of other outbreaks (eg, Nipah, MERS, and the 2002–04 SARS outbreak) direct evidence for a natural origin for SARS-CoV-2 is missing. After 19 months of investigations, the proximal progenitor of SARS-CoV-2 is still lacking. Neither the host pathway from bats to humans, nor the geographical route from Yunnan (where the viruses most closely related to SARS-CoV-2 have been sampled) to Wuhan (where the pandemic emerged) have been identified. More than 80 000 samples collected from Chinese wildlife sites and animal farms all proved negative. In addition, the international research community has no access to the sites, samples, or raw data. Although the Joint WHO-China Study concluded that the laboratory origin was “extremely unlikely”, WHO Director-General Tedros Adhanom Ghebreyesus declared that all hypotheses remained on the table including that of a laboratory leak.A research-related origin is plausible. Two questions need to be addressed: virus evolution and introduction into the human population. Since July, 2020, several peer-reviewed scientific papers have discussed the likelihood of a research-related origin of the virus. Some unusual features of the SARS-CoV-2 genome sequence suggest that they may have resulted from genetic engineering, an approach widely used in some virology labs.Alternatively, adaptation to humans might result from undirected laboratory selection during serial passage in cell cultures or laboratory animals, including humanised mice. Mice genetically modified to display the human receptor for entry of SARS-CoV-2 (ACE2) were used in research projects funded before the pandemic, to test the infectivity of different virus strains. Laboratory research also includes more targeted approaches such as gain-of-function experiments relying on chimeric viruses to test their potential to cross species barriers.A research-related contamination could result from contact with a natural virus during field collection, transportation from the field to a laboratory, characterisation of bats and bat viruses in a laboratory, or from a non-natural virus modified in a laboratory. There are well-documented cases of pathogen escapes from laboratories.Field collection, field survey, and in-laboratory research on potential pandemic pathogens require high-safety protections and a strong and transparent safety culture. However, experiments on SARS-related coronaviruses are routinely performed at biosafety level 2, which complies with the recommendations for viruses infecting non-human animals, but is inappropriate for experiments that might produce human-adapted viruses by effects of selection or oriented mutations.