All of the world's COVID vaccines are designed to train the body to recognize and respond to the SARS-CoV-2 virus's distinctive spike protein. Except now the spike protein seems to be changing rapidly to make the virus more easily transmissible and less likely to be thwarted by any of the current vaccines or by antibodies in or from previous COVID survivors. This seems to be driven by sloppy attempts to stamp out COVID in many spots around the world rather than by the travel of a single new strain. "That pattern is what scientists refer to as 'convergent evolution,' and it’s a sign of trouble ahead. All viruses mutate. ... For most of 2020, those random changes didn’t have much of an effect on the way the virus behaves. But recently, three notable mutations have begun to show up alone or in combination with each other. And everywhere they do, these versions of the virus tend to quickly outcompete other circulating strains. ... It may feel like the Covid-19 pandemic has been happening forever. But in evolutionary terms, it’s been but a blink. Before SARS-CoV-2 crossed into humans, it had been circulating inside bats for millions of years. And when scientists began taking a closer look at the bat version of ACE2, they found a staggering diversity of the gene that codes for that protein. What they were seeing were the genetic scars of an evolutionary arms race. Bat populations had lived with SARS-CoV-2 for long enough that their ACE2 receptors had started changing—morphing in shape so that they became harder for the virus to grab onto. And in turn, SARS-CoV-2 had evolved to try to fit into those new shapes. Eventually, one of those descendants looked enough like the human ACE2 receptor that it could make the cross-species leap (with perhaps an intermediary host in there somewhere). There are two major evolutionary forces driving diversification of the spike protein: interacting with ACE2, and getting clobbered by neutralizing antibodies. In the human population, a year isn’t long enough for new versions of ACE2 to crop up and be passed on to a new generation of people. And ACE2 plays a key role in regulating blood pressure, wound healing, and other essential functions, so any genetic changes that impair its ability to do those things would likely not get very far, even if they made it more difficult for the coronavirus to start an infection. ... So the obvious question is: Where did the virus encounter these antibodies? ... 'The fact that we lost control in so many places in the fall allowed for the ballooning of this incredibly huge viral population size,' says [University of Utah evolutionary virologist Stephen] Goldstein. That created the opportunity for that many more mutations to happen, and in some places, the right circumstances for some particularly insidious ones to get selected. [Harvard infectious disease epidemiologist William] Hanage put it this way to reporters last week: 'The strategy here and elsewhere has been to try and control the level of transmission that doesn’t require very severe restrictions, but also doesn’t allow the virus to go exponential and overload health care systems.' But the problem with that approach is that it still gives the virus plenty of opportunities to mutate, and in so doing, change its behavior. If those changes make it spread faster or give it an edge against treatments and vaccines, that balancing act falls apart. ... Hannage pointed to what’s going on right now in Manaus, a city in the Brazilian Amazon where a devastating surge in May left up to 70 percent of its residents infected with SARS-CoV-2, according to an analysis published this month in Science. Doctors and researchers there assumed the city was safe for a while—that herd immunity, or close to it, had been reached. But this month, the Manaus public health system collapsed again under a new Covid crush, leaving hospitals scrambling to get enough oxygen for its mass of patients. 'I’m not yet aware of any evidence to suggest that the P1 variant is more likely to infect or reinfect people,' said Hanage. 'But the fact that this is happening in a place that had previously been exposed to such high amounts of transmission is extremely worrying, very worrying indeed.' Scientists may never get a clear answer to exactly where and under what conditions these new variants emerged. But [South African geneticist and bioinformatician Tulio] de Oliveira isn’t so sure it matters. 'The one thing we know for sure is that if you keep the virus circulating long enough, it will develop escape mutations,' he says. ... [S]cientists like Hanage are still worried that if governments and societies don’t do enough to slow the speed of infections soon, more dangerous mutations will almost certainly emerge. 'The fact that it’s happened three times already means we can expect it to continue happening,' he said during last week’s press briefing. If you ask de Oliveira, he’ll tell you that it is already happening, and much faster than anyone realizes. 'I am quite convinced that there are dozens, if not hundreds, of variants with similar mutations emerging around the world right now,' he says. He believes that the only reason that South Africa and the UK picked them up first is because their governments invested in comprehensive surveillance networks."
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