Viruses have a singular goal: Get in, copy, copy, copy, get out.
But even with ample experience reproducing themselves, viruses still aren’t perfect at it. They make mistakes, like accidentally inserting one nucleotide for another, deleting one, or doubling another. These are known as mutations, and the result is daughter virions (virology speak for “units of viruses outside of host cells”) that aren’t quite clones. Often, these mutations aren’t a big deal. But when mutations prove particularly advantageous for the virus—i.e. help it replicate in some way—they become more prevalent. That leads to a new variant.
“If [mutations] don’t spread more, you don’t have to worry about it,” says Florian Kramer, a professor of microbiology focusing on infectious diseases at the Icahn School of Medicine. The challenge is evaluating the implications of the ones that do proliferate.
Scientists are now assessing whether certain mutations of the SARS-CoV-2 virus are helping it spread faster, evade antibodies from vaccines, or cause new infections. These variants first popped up in the UK, South Africa, Brazil, and California (respectively), and the fear is that they could worsen a pandemic already far from under control. “I don’t think it’s hyperbolic to say the worst could be yet to come,” Angela Rasmussen, a virologist at Georgetown University’s Center for Global Health Science and Security, told ProPublica.
Most of the mutations scientists have observed so far are to SARS-CoV-2’s spike protein. This protein is the target of all the vaccines available and in the pipeline, because it’s both the crowbar with which the virus enters our cells, and the virus’s signature molecular look. The spike protein is made of nearly 1,300 amino acid blocks, and mutations in the virus’s RNA (a single strand of genetic material) can result in changes in some of these amino acids.
For example, the UK variant, or B.1.1.7., is a set of handful of mutations whose change to the spike protein makes the virus stickier. Because this variant has a stronger hold on our cells, a smaller viral load can cause an actual infection. Thus, the virus becomes more transmissible. Estimates suggest this strain is about 50% more transmissible than previous strains.
The South African strain, called B.1.351, is similar to B.1.1.7. but with a few additional mutations on the spike protein, including one called E484K, or “EEEK” for short. In pre-prints, scientists have found that this mutation may make it harder for antibodies to neutralize the virus.
The variant first found in Brazil, called P.1, shares some of the same spike protein mutations as the South Africa and UK variants. Scientists aren’t sure why, but it seems like there are some mutations in the P.1 variant that may make this strain capable of reinfecting individuals. Normally, health officials would assume that people who have already been sick with Covid-19 have some protective immunity.
Last month, scientists in California identified another variant. This one, called CAL.20C, appears to have made up a quarter of cases in Southern California in October. Although it contains mutations on the spike protein, they’re not the same as any of those previously described. Scientists are still working out if these mutations have any tangible effect on the virus or the infection it causes.
Variants can also acquire new mutations. Scientists have occasionally peeped the EEEK mutation on the UK and Brazil variants; they’ve also witnessed evidence of recombination, a process by which the SARS-CoV-2 virus can move around entire sections of its genome as it replicates. It’s unclear, however, how much recombination is contributing to new kinds of variant formation.
The B.220.127.116.11 variant has made its way into 50 countries or territories so far, including the US, where the Centers for Disease Control and Prevention (CDC) predicts it will be the dominant strain in just a few weeks. The B.1.351 variant has appeared in 30 countries; and the P.1 variant has been found in Brazil and Japan, after tourists returned from visiting the former.
Scientists worry these variants are already in more places than we think. Finding variants and assessing their prevalence requires genetic sequencing after a patient provides a positive PCR test, but the US is only sequencing about 1% of its variants, according to ProPublica. As of late January, it was 38th in the world for sequencing. The CDC has contracted with private companies to try to raise this rate. As of December 2020, Australia was leading with 43% of its cases sequenced, but no country is capturing 100% of cases.
That’s the million-dollar question.
For the most part, these mutations don’t make the SARS-CoV-2 virus that different from previous strains, which means most vaccines should be somewhat protective against them. Even if a vaccine can’t protect against all cases, the initial immune response should be enough to tame would-be severe ones.
And so far, there is limited evidence that any of these variants make Covid-19 infections more severe. In the case of B.18.104.22.168, more people could get sick—which may have an impact on hospitalizations and ICU rates. And while data suggests B.1.351 and P.1 may be able to avert neutralizing antibodies, they still shouldn’t make people sicker.
“It’s a huge relief to know that the vaccines still seem to protect against hospitalization and deaths,” Emma Hodcroft, a molecular epidemiologist at the University of Bern, told STAT.
That said, the B.1.351 variant in particular is giving some vaccine and therapeutics companies pause. Earlier this week, the South African government halted deployment of the AstraZeneca vaccine after a preliminary study showed it to be less effective against the new variant. Janssen also reported that its single-shot vaccine prevented 57% of cases in South Africa, compared with 66% on average, and Novavax found that its double-shot vaccine only prevented 49% of cases, versus nearly 90% elsewhere. There’s no data on whether the Pfizer-BioNTech and Moderna vaccines will work well against this variant yet—they were tested before it was prevalent—but Moderna has said it’s testing boosters for it presently. Regeneron also updated its monoclonal antibody treatment after finding it to be less effective against viruses with the EEEK variant.
All that uncertainty highlights why it’s still best to avoid getting Covid-19 at all, which means staying vigilant with the same old pandemic precautions: hand-washing, physical distancing, and wearing a mask (or two) when inside public spaces. ”If anyone asked me half a year ago, I would have said the virus is pretty stable,” says Krammer. Now there’s no guarantee the mutations will stop.