![]() That happens with influenza but is fairly new to SARS-CoV-2. Seeing so many lineages of the coronavirus develop similar constellations of genetic changes at these spots is a sign of convergent evolution – when versions of the virus have slammed into the wall of immune defenses in the human population, and then come up with ways to get around them. Instead of a Greek alphabet, scientists are maintaining shortlists of worrisome spots for mutation: 346, 444, 445, 452, 460, 486, 490. The coronavirus spike protein is made up of about 1,300 building blocks called amino acids, and mutations that change even a single building block can make it harder for antibodies to block the virus. Instead of worrying about which variant will win, or even focusing on particular mutations, many scientists have shifted to watching hotspots – specific sites on the virus, known by numbers like a street address, where any change in the virus’s code might allow it to slip by the neutralizing antibodies that are a first line of defense. “It’s important for people to understand that the fact there’s not a Greek letter name that has come out does not mean the virus stopped evolving,” said Jesse Bloom, an expert on viral evolution at Seattle’s Fred Hutchinson Cancer Center, who described the evolutionary rate of SARS-CoV-2 as “strikingly rapid.” And then there’s this: Monoclonal antibodies, targeted drugs that can be used as a treatment or to protect immunocompromised people who don’t respond well to vaccines, are likely to be knocked out by future variants. But protection is fleeting for two key reasons: immunity wanes and the virus is changing. That protection gave us the relative freedoms of the moment – with many people returning to normal life. Much of the world’s population has gained a measure of immunity because of vaccinations and omicron infections. ![]() That doesn’t mean they think the virus is standing still. ![]() Most virologists demur when asked about which variant – or variants – will be infecting people this winter. Each mutation gives the virus a leg up in avoiding this primary line of immune defense. If those antibodies can’t dock, they can’t block. What matters is all these new threats are accumulating mutations in similar spots in what’s called the receptor binding domain – a key spot in the spike protein where virus-blocking antibodies dock. To focus too much on any one possible variant is, many experts argue, missing the point. A lineage called XBB looms on the sidelines, and threatens to scramble the forecast. A few weeks ago, BQ.1.1 started to steal the spotlight – and still looks like a contender to take over this fall in Europe and North America. In the United States, BA.4.6 and BF.7 have been slowly picking up steam. A month ago, scientists were worried about BA.2.75, a variant that took off in South Asia and spawned a cloud of other concerning sublineages. The pace of evolution is so fast that many scientists depend on Twitter to keep up. “It is this constant evolutionary arms race we’re having with this virus,” said Jonathan Abraham, an assistant professor of microbiology at Harvard Medical School. ![]() Each new subvariant seems to outdo the last in its ability to dodge immune defenses. They are different flavors of omicron, but eerily alike – adorned with a similar combination of mutations. ![]() Instead, one or more of the multiple versions of the omicron variant that keep popping up could drive the next wave. This time, it’s unlikely we will be barraged with a collection of Greek alphabet variants. For two years, coronavirus variants emerged, one by one, sweeping the globe.īut this fall and winter are expected to be different: Instead of a single ominous variant lurking on the horizon, experts are nervously eyeing a swarm of viruses – and an evolutionary phase in the pandemic. ![]()
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