(CN) — As people around the world have had to adapt their lives to the presence of Covid-19, the virus causing the illness, too, has been morphing to make the most of its situation.
Mutations that give way to emerging coronavirus variants remain a key factor in the race to vaccinate all American adults and curb the pandemic. Our existing vaccines seem to neutralize the most prominent variant in the United States, but not all virus mutations work the same way, opening up the possibility of a vaccine-resistant virus showing up in the future.
Researchers agree that widespread vaccination — with continued mask-wearing and social distancing along the way — is vital to winning the race. What’s less clear at this point is how policy should reflect the ever-changing science on coronavirus variants, including how the science behind different variants can influence its spread.
A snapshot of the latest science, and still-developing matters of policy, offers the hope of vaccination progress, while making clear that unanswered questions will ultimately decide the pandemic’s future.
Science Behind Mutations
Like all viruses, SARS-CoV-2 is able to replicate only inside a host organism. So the virus’s ultimate goal, its means to survive, is to spread as efficiently as possible.
To achieve increased transmissibility, viruses mutate constantly. When a beneficial mutation appears in a virus’s genes, it’s likely to take over as the dominant version.
But mutations can arise in different parts of the genome, and the various ways in which a virus becomes more transmissible can change what a variant means for human health.
In the United States, for example, officials from the Centers of Disease Control and Prevention reported last week that the country's most prominent variant — B.1.1.7, which originated in the United Kingdom — accounts for more than a quarter of U.S. cases and was the predominant strain in at least five regions.
That doesn’t come as a surprise: The CDC had predicted a takeover of the strain known to be 50- to 70% more transmissible than what is known as the “wild type,” SARS-CoV-2.
Stephen Kissler, a postdoctoral researcher studying immunology and infectious diseases at Harvard T.H. Chan School of Public Health, explained how the variant spreads more easily on a “per-contact basis."
“That probably has something to do with the way the virus interacts with our body’s cells,” Kissler said: It’s just easier for it to invade.
But the P.1 variant, first identified in four travelers from Brazil during routine airport screening in Tokyo, uses a different strategy.
The Brazilian variant may not be more infectious in general, Kissler said, but it “really thrives in places where we’ve already seen a lot of infections.”
“Where previous immunity would keep other types of variants out, the P.1 can spread more easily because it gets around the immune system,” he explained.
Viruses can also evolve to cause more severe illness. That’s not necessarily advantageous to a virus, which cannot spread if it kills its host.
“But sometimes the same mutations that cause increased transmissibility, like better binding to our body’s cells, can create some more severe clinical manifestations, just sort of as a byproduct,” Kissler said. “And so that’s something that we have to watch very closely as well.”
When SARS-CoV-2 enters the body, it binds to receptors in the lung cells to gain access to the rest of the body, “hijacking our cellular machinery.” Binding more tightly, Kissler said, not only helps the virus spread — but can also infect more cells within one person, worsening the virus’ effect.