Organisms mutate. That’s often a good thing. If it weren’t for mutations, we might all still be single-celled organisms clinging to hydrothermal vents in the ocean’s black depths.
Mutations – random, inevitable changes to life’s genomic code – don’t always turn slime into Shakespeare, though. Viruses mutate also.
SARS-CoV-2, the virus behind the COVID-19 pandemic, is no exception. The coronavirus’s RNA genome consists of about 30,000 base pairs. Since Chinese scientists first decoded the virus’s genetic code in December, it has accumulated an average of one or two random mutations a month. One in particular, called D614G, may well have boosted disease’s infectiousness.
That particular coronavirus mutation has raised questions about the future of the coronavirus – and, by extension, the possible impact on the civilization the virus has attacked.
Viral mutations come and gone
Viral mutations have been well documented. The 1918 Spanish flu pandemic was caused by a virus that mutated (probably from waterfowl who weren’t bothered by it) to infect humans. That virus, H1N1, hung around in people until 1957, when some combination of mutations and increasing immunity caused it to fade from our species. In 1977, a mutated version of H1N1 emerged again and jumped from pigs to humans in China. The same thing happened in 2009, causing the H1N1 swine flu outbreak. That H1N1 strain still circulates as a seasonal flu virus whose mutations have now changed fully 15 percent of the original Spanish flu genome. The good news: in general, H1N1 has become less virulent with time.
That’s not by chance. If you’re a virus with the sole goal of proliferating as widely as possible, mutating to cause a mellower infection makes sense. (Even HIV may be evolving into a less-dangerous form.)
“In general, viruses do want to replicate better and faster and spread themselves faster,” said Dr. Thomas Campbell, a University of Colorado School of Medicine and UCHealth infectious-disease specialist.
But other flu types have mutated less happily for humans. H3N2, another seasonal flu, originated in Hong Kong in 1968 and has mutated such that the antibodies that normally alert our immune system to the virus have a hard time binding to it. H3N2 influenza now almost universally has that mutation, one was first detected during the 2014-2015 flu season.
The D614G coronavirus mutation spread even faster. At some point earlier this year, an A changed to a G at position 23,403 of the coronavirus’s RNA genome. It was a classic random mutation, one that could have hurt the virus’s fitness, helped it, or made no difference at all. In this case, the mutation subtly changed the shape of the necks of the spike proteins protruding from it.
One research team investigating the mutation in a lab has concluded that the change made the spike stronger and therefore better able to maintain its shape and bind like a key to the lock of a human cell’s ACE2 receptors. That team’s conclusion followed that of the team that had reported the mutation in the journal Cell. The mutation made the G614 version of the coronavirus perhaps 10 times more likely to spread, cell-for-cell in a lab setting, than the original D614 coronavirus that took root in China.
Today, pretty much every coronavirus case has the G614 mutation.
Bad news and good news about coronavirus mutation
In a commentary accompanying the Cell study’s findings, scientists noted that the new variant’s vastly greater infectiousness in the lab doesn’t necessarily translate into the same thing in the noses and lungs of human beings. In addition, the G614 mutation that became dominant could also have done so through random chance – combined with the fact that Chinese spread of disease with the D614 variant had slowed to a trickle by the time the G614 version was rampaging through Europe, the United States and beyond. But from what we know about Darwinism, the mutation probably conferred a competitive advantage.
If the bad news is that the mutation probably makes the coronavirus more infectious and therefore hard to stop its spread, the good news is that the mutation doesn’t appear to make the disease of COVID–19 more severe. And while D614G mutation changes slightly the shape of the coronavirus’s notorious surface-spike proteins, the change doesn’t appear to impact the binding site atop of the protein spike. That binding site is what SARS-CoV-2 viruses use to unlock human cells – and it’s also the primary target of the most promising vaccine-development efforts.
“The mutation seems to have spread more rapidly around the world than the original virus that was first described in Wuhan, China, in December,” Campbell said. “As far as we know, this specific mutation should not affect the efficacy of vaccines as it’s not located at the part of the spike protein where vaccines would have their specific effect.”
Mutations can bedevil vaccine developers, though, says Campbell, who is leading the Colorado site of the major Moderna vaccine trial.
Mutations have been “a huge issue for developing an HIV vaccine, and it’s also an issue with influenza vaccines,” Campbell said. “It’s a big reason why we have to have a different flu shot every year.”
Thanks to built-in error-correction, the novel coronavirus mutates slower than HIV and influenza viruses. That doesn’t necessarily translate into an easier path to a vaccine – any more than rapidly mutating viruses such as measles thwarted vaccine developers.
For now, the coronavirus has no need to evolve anyway. In a few short months, SARS-CoV-2 has taken up residence in all corners of the planet (save, for now, Antarctica). It took the single-celled vent-dwellers that became ants, oak trees, and us about four billion years to do the same.