Houston researchers have unveiled a study of over 5,000 genetic sequences of coronavirus which reveals the pathogen's virus's continuous accumulation of mutations.
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The study, released on September 23, however, does not conclude that these mutations made the virus deadlier or changed clinical outcomes. According to scientists, all the viruses accumulate genetic mutations and most of them are insignificant, The Washington Post reported.
Study author James Musser of Houston Methodist Hospital said that coronaviruses like SARS-CoV-2 are relatively stable as viruses go since they have a proofreading mechanism as they replicate. "But every mutation is a roll of the dice, and with transmission so widespread in the US -- which continues to see tens of thousands of new, confirmed infections daily -- the virus has had abundant opportunities to change, potentially with troublesome consequences," Musser said.
"We have given this virus a lot of chances. There is a huge population size out there right now," he added.
Several scientists from Weill Cornell Medicine, the University of Chicago, Argonne National Laboratory and Austin's University of Texas also contributed to the research. The study, which has not been peer-reviewed, appears to be the largest single aggregation of genetic sequences of the virus in the US as of now. Last month, a study by UK scientists said a mutation that changes the structure of the "spike protein" on the virus's surface may be driving the outsized spread of that particular strain, according to The Washington Post.
According to the new Houston study, the findings pointed out the strong possibility that the virus, which moved through the population, became more transmissible, and this "may have implications for our ability to control it", said David Morens, a virologist at the National Institute of Allergy and Infectious Diseases. Morens said it is a single study and "you do not want to over-interpret what this means." However, the virologist stated that the virus could be responding potentially through random mutations to such interventions as social distancing and wearing of masks.
"Wearing masks, washing our hands, all those things are barriers to transmissibility, or contagion, but as the virus becomes more contagious it statistically is better at getting around those barriers," Morens said, adding it could have implications regarding the formulation of vaccines. The virus could be under selective pressure to evade the human immune response as people gain immunity either through infections or a vaccine. "Although we do not know yet, it is well within the realm of possibility that this coronavirus, when our population-level immunity gets high enough, this coronavirus will find a way to get around our immunity. If that happened, we would be in the same situation as with flu. We will have to chase the virus and as it mutates, we will have to tinker with our vaccine," Morens said.
According to the study, the virus spread in two waves across neighbourhoods in Houston -- firstly affecting wealthier and older individuals and then spreading to younger people and lower income areas -- infecting several Latino city residents. Genetic data showed that the virus arrived in Houston many times, possibly by air travel first. Notably, 71 percent of the viruses which arrived initially were characterised by a now famous mutation, which appears to have first originated in China, that scientists believe could give the virus a biological advantage in how it spread, The Washington Post reported.
It is called D614G, referring to the substitution of an amino acid called aspartic acid (D) for one called glycine (G) in a region of the genome that encodes the spike protein. By the second wave of the outbreak in Houston, the research noted that this variant leaped to 99.9 percent prevalence. People infected with the strain had higher loads of virus in their upper respiratory tracts, which is a potential factor in making the strain spread effectively more, researchers found. According to Musser's interpretation, D614G was increasingly dominant in Houston and other areas as it was better adapted to spreading among humans. He acknowledged that the scientific case is not yet closed on the matter.
"This is not a murder trial. We are not looking for beyond a reasonable doubt. This is a civil trial, and clearly, it is the preponderance of the evidence that I think forces all of us into the same conclusion, which is there is something biologically different about that strain, that family of strains," said Musser.
Kristian Andersen, an immunologist at the Scripps Research Institute in California, downplayed the research's significance, saying it "just confirms what has already been described -- G increased in frequency over time."
Andersen, who was not involved in the study, said as for numerous other mutations, "they just catalogue them, but we do not know if any of them have any functional relevance." The study characterises some of the spike protein mutations as "disconcerting". Although the research does not show strong proof that additional evolution of the spike protein is taking place, it suggests "these repeated substitutions provide a hint as the virus interacts with our bodies and our immune systems, it may be learning new tricks that help it respond to its host". "I think there is pretty good evidence that is consistent with immunologic selection acting on certain regions of the spike protein," Musser was quoted as saying.
