“Voilà! It was just this huge increase in viral transduction.”
Scientists have been hard at work unraveling the mysteries of SARS-CoV-2 since January, when Beijing finally shared a mapped genome with the global scientific community (though early research also filtered out via the British journal “The Lancet”). At this point, scientists around the world have examined hundreds of thousands of viral samples from around the world. They’ve compared and contrasted their genetic code, and they’ve identified what appears to be an important pattern. That is: the earliest version of the virus that spread in Wuhan is not genetically identical to the iteration that went on to conquer Europe and the US.
According to a Bloomberg report comparing the findings from four non-peer-reviewed studies, it appears that a notable mutation of the virus that emerged broadly and early during its global campaign helped render COVID-19 more infectious in later iterations than it was during the early weeks of the outbreak, raising fears that the virus could continue to evolve in a way that eludes scientists working on a vaccine, or simply makes the virus more deadly.
At least four laboratory experiments suggest that the mutation makes the virus more infectious, although none of that work has been peer-reviewed. Another unpublished study led by scientists at Los Alamos National Laboratory asserts that patients with the G variant actually have more virus in their bodies, making them more likely to spread it to others.
The mutation doesn’t appear to make people sicker, but a growing number of scientists worry that it has made the virus more contagious.
“The epidemiological study and our data together really explain why the [G variant’s] spread in Europe and the U.S. was really fast,” said Hyeryun Choe, a virologist at Scripps Research and a lead author of an unpublished study on the G variant’s enhanced infectiousness in laboratory cell cultures. “This is not just accidental.”
Another team of researchers described the feeling of shock when they realized just how much more effective this mutation made the virus in terms of its ability to break into human cells.
Neville Sanjana, a geneticist at the New York Genome Center and New York University, was trying to figure out which genes enable SARS-CoV-2 to infiltrate human cells. But in experiments based on a gene sequence taken from an early case of the virus in Wuhan, he struggled to get that form of the virus to infect cells. Then the team switched to a model virus based on the G variant.
“We were shocked,” Sanjana said. “Voilà! It was just this huge increase in viral transduction.” They repeated the experiment in many types of cells, and every time the variant was many times more infectious.
The mutation in question is known as D614G, or just “G” for short. So far, the “G” mutation has been found in roughly 70% of the half a million or so samples that have uploaded to a shared database for scientists around the world. This has convinced many scientists of its significance, especially because the mutation occurs in a part of the genome that governs the infamous “spike” protein that gives the virus its name (“corona” = crown in Latin) and is believed to enable it to infiltrate human cells.
“I think that slowly we’re beginning to come to a consensus,” said Judd Hultquist, a virologist at Northwestern University.
And although it won’t help the quest for a cure, understanding the role of these mutations is critical for understanding how the virus works. This, in turn, would allow scientists to track mutations and help them discern which might enhance the virus’s capability to destroy human life.
“Understanding how transmissions are happening won’t be a magic bullet, but it will help us respond better,” Sabeti said. “This is a race against time.”
Though, to be sure, even with all the research that’s been done so far, scientists can’t say much, if anything, for certain about the mutation. There may be other explanations for the G variant’s dominance in the global pandemic: perhaps biases in where genetic data are being collected has led it to be overrepresented in samples, or quirks that led the “G” variant to dominate in particularly susceptible populations.
“The bottom line is, we haven’t seen anything definitive yet,” said Jeremy Luban, a virologist at the University of Massachusetts at Amherst.
Remember that the next time you hear Trump, Dr. Fauci or the White House “vaccine czar” discuss the possibility of having a vaccine available by year end, or next time you see a country contract to buy millions of doses of Gilead’s remdesivir, just keep this in mind.
The statements, views and opinions expressed in this column are solely those of the author and do not necessarily represent those of The Duran.