The experiments proposed in this grant would likely not pose the risk of releasing a new pandemic strain of coronavirus. Speaking as someone who has worked in labs that study RNA viruses, there are ways to perform these studies in a safe manner. To study how mutations in the spike protein affect cell entry, scientists create something called a
pseudotyped virus. This is essentially taking the spike protein from the coronaviruses that you'd like to study, and putting it on the outside of what is essentially a harmless virus shell. Typically, researchers use
lentiviral vectors, which are derived from HIV. These viruses have been extensively modified to prevent them from being able to reproduce, so once the virus enters the cell, it cannot make new copies of itself (see the Addgene link above for more details). This technology is routinely used in many biomedical research labs to introduce foreign genes into cells. These types of experiments using pseudotyped viruses have been done with SARS-CoV-2 spike protein in many published studies (for example,
studying which antibodies are able to bind the SARS-CoV-2 spike protein to prevent viral entry). So, this one sentence does not necessarily mean that the researchers were engaged in dangerous gain of function experiments.
Newsweek, however, does report that gain of function studies on bat coronaviruses did occur at the Wuhan Institute of Virology. They write:The article seems to be referring to this
2015 publication in Nature Medicine. As the Newsweek article notes, genetic analysis of the viral RNA would easily spot a virus generated through such gain of function studies, and the SARS-CoV-2 RNA sequence does not show signs of being manipulated in these ways.
The Newsweek article discusses the possibility that the virus could have evolved through passaging of the virus in laboratory conditions, which could adapt a bat virus to be more transmissible in human cells. Again,
genetic analysis of the viral RNA has identified various genetic features of the virus that enable its transmissibility in humans. One feature are a set of mutations in the receptor binding domain of the spike protein that help the spike protein bind to the human ACE2 receptor more strongly. These mutations are similar to mutations found in a Pangolin coronavirus, so these mutations were likely introduced naturally into the progenitor bat Coronavirus through recombination. The other feature is a polybasic furin cleavage site within the spike protein, which is not found in other related coronaviruses. It is certainly possible for such sites to evolve naturally, as many other viruses have evolved furin sites in their extracellular proteins (including the MERS coronavirus), though the exact origins of the SARS-CoV-2 furin site remains unknown. While evolution of furin cleavage sites has been observed in
laboratory passage of influenza virus, the SARS-CoV-2 sequence has other features (such as the introduction of a glycosylation site) that would not be expected to be selected for during passage in cultured cells, which would disfavor the laboratory passage hypothesis over a natural origin.
While the exact origins of the virus aren't known (and may never be known), most of the existing evidence supports a natural origin over an accidental release hypothesis. Indeed, we know of many new viruses that have jumped from animals to humans (e.g. HIV, ebola, swine flu, avian flu, Zika virus), including two new coronaviruses that have emerged within the past two decades (the original SARS and MERS). Ultimately, extraordinary claims require extraordinary evidence. While we can't disprove the hypothesis that the virus escaped from a lab, I have not seen any compelling evidence to favor the laboratory escape hypothesis over a natural, zoonotic origin of the virus.