Researchers at Boston University (USA) have faced criticism for having created an artificial type of coronavirus. They inserted a protein from the surface of the Omicron BA.1 variant virus into the “body” of the Wuhan variant virus extracted from a Washington patient in 2020, in the first outbreak of Covid-19 in the country.
In a small number of laboratory mice, the hybrid appeared to have high lethality, up to 80% — but the sample is too small to claim that this is the magnitude of lethality in rodents. It is important to note, however, that while the Wuhan variant is more lethal in these animals than the hybrid virus, the Ômicron variant caused only mild disease, without killing.
The inserted protein is the protein from spike or S protein, which acts as a key opening a lock to allow the virus to enter the cells of the parasitized organism. Compared to the “pure” virus of the Ômicron variant, the hybrid is much more efficient at replicating: the mice produced 30 times more virus when infected with the latter.
In the news section of Boston University itself, the leader of the laboratory that carried out the study, Ronald Corley, complains of sensationalism in the coverage of the research in the press, especially in the British newspaper Daily Mail. “They misrepresented the study and its goals completely,” said the scientist. He explains that the intention was to assess which part of the virus is most responsible for making the infected organism sick. It does not appear to be the spike protein, and that would be the main result.
The results of the study are in a bank of pre-press articles, which are those that have not yet gone through the review process by peers, widely adopted as a prerequisite for publication in scientific journals. The pre-press article has been available since 14 October.
In May 2021 research that potentially makes viruses more infectious in humans, an effect called “gain of function”, had funding cut by the National Institutes of Health (NIH). Before, between 2014 and 2017, the Obama administration imposed a moratorium on this type of research. There was, however, a loophole: authorities such as Anthony Fauci and Francis Collins could make an exception for specific recipients of the grants.
Boston University denies that the study qualifies as gain of function, as it “did not amplify” the Washington strain, “nor make it more dangerous”. For Steven Salzberg, a biomedical engineering expert and columnist for Forbes magazine, the university’s denial makes no sense, and it wanted to change the definition of “gain of function” while denying that research did. For him, it is clear that it is a gain of function because a more lethal and more infectious strain was generated than one of the mother strains. It is not known what effect this hybrid coronavirus would have on humans. “I hope we never find out,” Salzberg commented in his column.
For virologist Valentin Bruttel, from the University of Würzburg in Germany, “any terrorist group could copy the protocols” of the research, which in his opinion of it is useless and dangerous because it gives the opportunity to form a recombination of different variants that would not happen in nature.
The NIH told The Hill that they are investigating whether the Boston University study fits in gain of function. NIH officials said they were not informed in advance of the survey. The university, publicly criticized by the agency, defends itself by saying that the protocol passed through its research ethics committees.
The NIH’s position, however, can be contradictory. Recently, the body, the largest research funder in the United States, announced a renewal of funding for the NGO EcoHealth Alliance to investigate more “emerging pathogens”. In recent years, the NGO has been an intermediary for funds between the US government and the Wuhan Institute of Virology, which has carried out gain-of-function research and is one of the main candidates in the hypothesis of the laboratory origin of the pandemic coronavirus.