The coronavirus variants are, in a word, confusing.
By now, you have likely heard about different variants that first raised trouble in the United Kingdom, South Africa, Brazil, and now maybe California — though the jury is very much out on whether that last one is cause for concern. To make a messy alphabet soup even more jumbled, these variants have unwieldy names, and they each contain mutations with unwieldy names of their own. The result is that people are left trying to differentiate among B.1.1.7 and N501Y and E484K and C-3PO.
Wait, sorry, that last one is from “Star Wars.”
The point is that all of this is difficult to keep track of, and it will only grow more confusing with more variants likely to turn up. “It’s becoming a mutation-of-the-week game,” said Stephen Goldstein, a coronavirologist at the University of Utah.
Below, STAT explains what’s known about the variants, why they’re getting so much attention, and what they mean for the trajectory of the pandemic.
Why are variants popping up now?
Well, they are and they aren’t.
SARS-CoV-2, the virus that causes Covid-19, has been mutating all along; that’s just what viruses do. Many of those mutations don’t change the virus substantively, and some might actually be detrimental to the virus, making that variant likely to die out.
But every so often, a mutation or combination of mutations will give rise to a new form of the virus with an evolutionary edge, like being able to infect cells better or spread faster. This new variant can outpace earlier iterations of the virus and become dominant.
Early on in the pandemic, a mutation known as D614G seems to have given the virus a boost in its infectiousness, and variants with the mutation became the most prevalent around the world.
Beyond the fact that the virus is constantly changing, there are other reasons why these “fitter” variants have started to emerge. In the early days of the pandemic, when just about all of us were vulnerable to Covid-19, any infectious variant had a pretty easy time circulating. But as more people in certain areas have become protected — either after an initial infection or vaccination — pressure on the virus has increased. A so-so spreader might no longer be able to find new hosts (that’s us) to infect, but variants with mutations that help them spread can still transmit, and can take off from there.
“We’ve reached a point one year on and in certain parts of the world where the density of natural immunity is sufficient so that the variants that have got a fitness advantage … are more likely to emerge and spread,” said Wendy Barclay, the head of infectious diseases at Imperial College London.
From the time SARS-2 got on people’s radars in late 2019, it was already quite well-suited to infecting humans, even compared to SARS and MERS, the other coronaviruses that have caused health emergencies in recent decades. But that’s not to say that SARS-2 didn’t have room to improve.
“Compared to SARS or MERS, it was already quite capable, but that doesn’t mean that it couldn’t become more capable,” said Kristian Andersen, an infectious diseases expert at Scripps Research Institute. “And that’s what we’re observing now.”
The variant that first appeared in the U.K. — and perhaps others as well — is a bit of a special situation. Most people who have an acute case of Covid-19 will vanquish the virus after a relatively short period of time. But it’s thought that this variant, dubbed B.1.1.7, came from a person who was immunocompromised and had a rare chronic case, essentially providing an incubator for the virus to accrue mutations as it replicated for weeks or months in that person’s body. The virus, the hypothesis goes, then spread from that person to others.
If the virus is changing all the time, why are these variants setting off alarms?
For now, let’s focus on the variants that emerged first in the U.K., South Africa, and Brazil. (There are at least two variants in Brazil scientists are keeping an eye on). These have the most evidence of greater transmissibility or some other characteristic that might be cause for concern. And, what’s more, they share some of the same mutations despite arising independently. To scientists, that’s a clue that the mutations might confer some evolutionary advantage.
When scientists assess the impact of a new viral variant, they consider at least three factors: disease severity, protection, and transmissibility.
For now, none of the variants seems to change how sick people get with Covid-19.
Answering the question of whether people with existing immunity to SARS-2 are still protected — and whether the vaccines still work — is a bit more complicated. Scientists are testing vaccines against the mutations and variants, and results should be available in the coming weeks. But many experts have a fairly optimistic outlook on the vaccine question. The vaccines generate a multipronged immune response that recognizes and targets different parts of the virus; changes caused by one mutation likely won’t make the virus invisible to protective antibodies generated by immunizations. And even if a mutation reduces the vaccines’ effectiveness a bit, the shots have been shown to be so powerful that they should work just fine even if their potency is taken down a notch.
Eventually, scientists think, the virus will accumulate the right combination of mutations to warrant updating the vaccines, a not-that-difficult process for vaccine makers. But it doesn’t appear we’re at that point now (though plenty of studies are ongoing, and some are more anxious than others).
There are some concerns about people becoming more vulnerable to reinfection with the new variants. In lab experiments, one of the mutations present in the variants identified in South Africa and Brazil, called E484K, has helped the virus evade the antibodies generated after an initial infection in some people.
On Monday, scientists in South Africa reported that antibodies from some people infected during the country’s first wave failed to recognize the newer variant spreading there now; they didn’t have results yet about its impact on vaccine-elicited antibodies. Separately, in Brazil, surging cases in a region that had already been hit hard by the virus raised worries that a different variant, called P.1, is able to sneak past existing protection and infect people again. (More on that in a second.)
When it comes to transmissibility, it seems that these variants do spread more easily — though there are wide-ranging estimates for just how much more infectious they are.
What does a more transmissible virus mean?
Because a more transmissible variant can infect more people more quickly, it leads to more cases overall without mitigation efforts. Even if people individually aren’t likely to get sicker, the result is that there will be more hospitalizations and deaths. (One caveat: Widespread vaccinations could prevent some of those.)
Faster-spreading viruses also require a greater proportion of a population to be protected for herd immunity to be achieved. Vaccine campaigns will have to reach even more people.
That also means that more contagious variants can spread in communities that, even if they hadn’t hit herd immunity, had enough immune people to blunt the circulation of SARS-2.
The arrival of more transmissible variants is “bad news, because that means some places that had already started to see protective effects become vulnerable again,” said Caitlin Rivers, an infectious diseases epidemiologist at the Johns Hopkins Center for Health Security.
What’s happening in Brazil?
A recent study estimated that three-quarters of residents of the city of Manaus, Brazil had been infected by SARS-2 by October. The hope was that this level of protection might act as a buffer against more transmission. But last month, cases started rising in the city and its state of Amazonas, straining local health systems once again.
When researchers dug into the viral sequences, they found many cases involved a new variant, called P.1, as reported last week. (P.1. has also been identified in people who traveled from Brazil to Japan.) They warned the mutations it contained (including E484K) are “potentially associated with an increase in transmissibility or propensity for re-infection of individuals.”
Scientists suspect there are several potential factors at work in Manaus, which could be playing out together. They’re investigating.
Maybe P.1 is indeed able to evade some existing immune protection, leaving people more susceptible to reinfection. Scientists on Sunday confirmed a case of reinfection caused by P.1 in Amazonas.
Or perhaps P.1 is so transmissible that it can spread just fine even in communities with 75% protection.
Or what if some people in Amazonas who were infected months ago are just generally becoming susceptible again to any form of reinfection, regardless of variants? Though immune responses vary, it’s thought that most people who fend off the virus will have lasting protection for some time — but that it will wane. Already, some reinfections have been reported around the world, without the involvement of more transmissible variants. (It’s thought that reinfections with SARS-2 will generally be milder for most people than their initial case because they still have some immune memory to the virus, even if their systems couldn’t block infection entirely. Scientists will be looking out to see if that holds with different variants.)
What are scientists doing about all this?
Studying it from all angles. One line of inquiry is examining the effects of mutations in isolation and in concert with the other changes dotting the virus’ RNA genome. Essentially, a mutation on its own may not have much of an impact, but it can help a virus spread better or replicate faster if it’s paired with certain other mutations.
Scientists are also on the lookout for other potential variants of concern as they comb through sequencing data. But there’s a sense among some experts that new variants are being announced without much helpful information. Lots of mutations will be discovered; it can take some time to figure out what, if anything, each one means.
In California, for example, officials held a press conference Sunday to discuss the L452R variant, which has grown from accounting for 3.8% of samples sequenced in the state in the first half of December to 25.2% of sequences heading into January. “We do not know whether it’s more infectious yet,” UCSF virologist Charles Chiu said, though he added, “it is concerning that it may potentially be more infectious.”
Outside experts were quick to say that more evidence is needed before such a claim can be verified. The variant was first seen in California in May, and hovered at low levels while the state was at low levels of virus overall. Then, it started to increase as the state was suffering from major outbreaks. This can create the illusion that the variant — because it’s so much more prevalent — was perhaps driving the cases. But without more data, it’s just as likely the variant didn’t cause the wave, but simply “went along for the ride,” Goldstein said.
And what can I do about it?
Commit to the same precautions that have been recommended for months, experts say. Perhaps invest in a better mask than a fabric face covering. Get vaccinated when you can.
Public health authorities have been stressing that the new variants aren’t solely responsible for the raging epidemics happening around the world. The United States has never really had a handle on its epidemic, and the most recent surge in cases was driven not by a more transmissible iteration of the virus, but because of lax policies and a lack of precautions.
“It’s too easy to just lay the blame on the variant and say, it’s the virus that did it,” Mike Ryan, the head of the World Health Organization’s emergencies program, said Friday. “Unfortunately, it’s also what we didn’t do that did it, and we have to be able to accept our share individually and as communities, as governments, our share of the responsibility in this virus getting out of control, while recognizing the variants in the virus make it difficult.”
The emergence of the variants has given experts a new line of argument in their regular pleas that people and governments should do all they can to drive down transmission generally. Slowing spread can buy time for more people to get vaccinated before one of the more transmissible variants becomes dominant — which could happen in the United States as soon as March, a model released by the Centers for Disease Control and Prevention last week showed.
And the more the virus spreads, the higher likelihood that even fitter variants will emerge. Evolution is driven not only by the environment the virus finds itself in, but also, as Barclay put it, “the number of times you roll the dice.”
Helen Branswell contributed reporting.