Since the start of the pandemic, SARS-CoV-2, the virus that causes Covid-19, has been mutating, its genetic code slowly changing as it spreads from person to person across the globe. For most of that time, the mutations didn\u2019t concern scientists. The genetic changes didn\u2019t seem meaningful in terms of how dangerous the virus is. Mutations are normal. Some even weaken the virus. <\/p>\n
Now, things are different.<\/p>\n
There are three mutated variants of SARS-CoV-2 of particular concern around the world. Researchers do not have the same level of evidence for each: One is more well understood than the others. But in each case, researchers see a seed of something concerning.<\/p>\n
There\u2019s B.1.1.7 (yes, all these variants are clunkily named). This variant was first detected in the UK in September. Scientists strongly suspect it\u2019s more transmissible (i.e., contagious) than past versions of SARS-CoV-2, and there\u2019s some preliminary evidence that it might be slightly more deadly. <\/p>\n
Then there\u2019s a pair of variants \u2014 one discovered in South Africa in October, and another in Brazil in December \u2014 that are less well understood. But scientists are beginning to suspect that they might have evolved ways to evade the human immune system, at least a little bit. <\/p>\n
A reasonable question you might be asking: Why now? Why have these three variants of concern popped up in such quick succession? The fact that the virus is mutating isn\u2019t new. It\u2019s been mutating all along. <\/p>\n
\u201cWe\u2019ve had many, many variants in SARS-CoV-2 for a long time now, and scientists have even been tracking these in fairly detailed ways since the summer of 2020,\u201d Emma Hodcroft, a molecular epidemiologist at the University of Bern, says. \u201cThe big difference is that, before December, we hadn\u2019t really seen any variants that seemed to be behaving any differently.\u201d (By \u201cbehaving differently\u201d she means that the virus itself didn\u2019t seem at the time to be more infectious, or more dangerous in any intrinsic way.)<\/p>\n
Hodcroft and others who study the evolution of viruses provide a few overlapping answers to the question \u201cWhy now?\u201d None of them perfectly explain what\u2019s going on. <\/p>\n
But thinking through them brings us to another, perhaps even more critical question: How might the coronavirus continue to evolve? Will even more variants emerge that challenge our fight against the virus? And what does that mean for the pandemic?<\/p>\n
Overall, experts outlined four reasons we\u2019re seeing these variants now. And it all boils down to one thing: evolution. <\/p>\n
Reason 1: The virus\u2019s genetic diversity increases over time<\/p>\n
First off, it\u2019s helpful to get a refresher on how evolution works. At its core, evolution requires two things: individual differences and natural selection. Evolution is a nonstop process. Organisms \u2014 as a group \u2014 accumulate change over time through mutations, and the environment helps determine which changes stick around in a population, and which become less prevalent. <\/p>\n
Viruses mutate because they\u2019re constantly making copies of themselves in enormous numbers. If you were writing a draft of something millions of times on a computer, extremely quickly, you\u2019d probably make some typos. This has happened millions and billions of times across the globe. The longer the pandemic rages on, the more chances the virus has to evolve. <\/p>\n
In the beginning of the pandemic, the viruses infecting people were really similar to one another, because they weren\u2019t that far removed from the original virus that began the outbreak. But now the virus has been changing genetically over the past year, branching out like a family tree. So many genetic changes have accumulated, in different places. <\/p>\n
\u201cWe have no evidence that the underlying mutation rate is changing,\u201d Sarah Cobey, an epidemiologist who studies viral evolution at the University of Chicago, says. The virus is still making its typos at the same rate. It\u2019s just that those changes start to accumulate the longer the pandemic continues. If you kept copying a book, over and over, making typos in each copy, you\u2019d end up with a somewhat different book than you started with. Likewise, according to Cobey, you\u2019d expect the genetic diversity of the virus to increase over time.<\/p>\n
So that\u2019s one major part of it. The virus has just had a lot of opportunities to become something slightly different. <\/p>\n
But that\u2019s not all of it. The increased diversity doesn\u2019t quite explain why we\u2019re seeing these particular \u2014 seemingly more concerning \u2014 variants at this particular time. \u201cWe are seeing evidence of adaptive evolution,\u201d Cobey says. These variants appear to be either getting better at infecting people or possibly evading the immune system, and they are doing so in similar ways.<\/p>\n
Genetic diversity alone doesn\u2019t explain that. Natural selection does. <\/p>\n
Reason 2: It\u2019s possible the virus is evolving in response to increasing human immunity<\/p>\n
The virus\u2019s increasing genetic diversity only explains part of the story. The other part of the story: natural selection. <\/p>\n
Some of the virus\u2019s genetic changes provide an advantage, which has led, in some cases, to these variants outperforming older strains of the virus. \u201cSome of those [genetic] substitutions are actually helping the virus replicate better,\u201d Cobey says, which then can lead to the variants infecting an increasingly larger proportion of people compared to other variants. <\/p>\n
Both the P.1 variant found in Brazil and the 501Y.V2 variant found in South Africa have a mutation called E484K, which changes the part of the virus that attaches to human cells (it\u2019s also the part that the immune system most readily recognizes after someone is vaccinated). That mutation, Hodcroft says, \u201cmight allow reinfection.\u201d In other words, people who have already been infected with SARS-CoV-2 could potentially be a little bit more susceptible to these variants (though this is still not confirmed). <\/p>\n
Hodcroft suspects that both the P.1 and 501Y.V2 variants may have evolved in response to human immunity. And she stresses: What follows is mostly speculative at this point. <\/p>\n
In the beginning of the pandemic, no human had been exposed to SARS-CoV-2 before. That means everybody\u2019s immune systems were equally bad at recognizing the virus. If there had been a variant that was good at evading the human immune system, it wouldn\u2019t have risen to prominence because it wouldn\u2019t have outperformed its viral peers. <\/p>\n
As Hodcroft explains it: \u201cEven if this [E484K] mutation popped up \u2014 which we know it did, we can see that it popped up a few times \u2014 it might not have been in a place where this was an advantage.\u201d<\/p>\n
In many places around the world, there are lots of people who have already been infected and who have developed some level of immunity to the virus. <\/p>\n
So now, variants that can evade the immune system have an advantage. They could grow and replicate where other variants cannot. And that variant could quickly become the dominant one. <\/p>\n
\u201cI want to be really clear: We aren\u2019t 100 percent sure, scientifically, that this is what\u2019s happened,\u201d Hodcroft says. \u201cBut these are the kinds of things to think about when we think about why we might be seeing different variants now. We\u2019ve changed the rules of the game.\u201d<\/p>\n
Reason 3: The virus has spread so far that rare things are starting to happen <\/p>\n
The longer the pandemic goes on, the more chances there are for rare \u2014 and sometimes consequential \u2014 things to happen. <\/p>\n
The B.1.1.7 variant might be one of these consequences. It appears to have acquired significant genetic changes over a short period \u2014 so many that scientists suspect the variant might have emerged in an immunocompromised person.<\/p>\n
In most people, Hodcroft explains, the immune system mounts a full-on assault on the virus, eliminating it in a couple of weeks. \u201cIn people that have compromised immune systems, though, there\u2019s a very different dynamic,\u201d she says. \u201cSo, for one thing, the virus could be in them for months instead of weeks.\u201d That gives the virus more time to evolve, to accumulate mutations that might make it easier to thwart the immune system.<\/p>\n
Many things have to happen for this to occur. Not only does an immunocompromised person have to get the virus (and many immunocompromised people are being particularly cautious), the virus would have to acquire mutations, and then the immunocompromised person would have to spread the virus to another person. <\/p>\n
\u201cThese are all like \u2018super-edge cases,\u2019\u201d Hodcroft says. But \u201cby keeping cases so high, you increase the chance that sooner or later, you\u2019re going to hit that jackpot … we keep rolling the die when we keep the cases up so high.\u201d<\/p>\n
Reason 4: Some Covid-19 treatments might have instigated some evolution<\/p>\n
The rise of these variants \u201cmay have something to do with the use of convalescent plasma,\u201d says Michael Worobey, the head of the department of ecology and evolutionary biology at the University of Arizona.<\/p>\n
Convalescent plasma treatments are blood plasma transfusions from people who have recovered from SARS-CoV-2. The idea is that along with the transfusion come antibodies that can help someone else with Covid-19 fight off the disease. The problem is that within certain recipients, the plasma could conceivably also create an environment that favors a stronger variant of the virus.<\/p>\n
\u201cSo there are cases where the identical [mutations] that characterize the UK variant have also evolved in patients who are chronically infected with the virus and were then given convalescent plasma,\u201d Worobey says. \u201cIt\u2019s a perfect storm.\u201d The virus has built up genetic diversity in the patient, and then the convalescent plasma acts as a force of natural selection, choosing among those variants one that could evade antibodies in that plasma. <\/p>\n
Worobey is not saying that this definitely happened with the B.1.1.7 variant, just that it\u2019s possible. (A similar thing, he says, could have happened with using monoclonal antibodies \u2014 synthetic antibodies produced as a Covid-19 treatment \u2014 on immunocompromised patients.)<\/p>\n
It\u2019s not that these treatments never <\/em>should have been used. In many cases, they may have helped save lives when there are few treatment options for Covid-19. But in the case of using convalescent plasma on immunocompromised people, Worobey says, it may have been \u201ca bit irresponsible.\u201d <\/p>\n The virus will keep evolving. Vaccinations need to happen quickly, and cases need to decrease.<\/p>\n The virus will keep changing, and there will be more variants. Not all will be variants of concern, though. <\/p>\n \u201cI think one thing that we definitely have to keep in mind, particularly in the next few weeks and months, is that a lot of people are now very interested in doing [viral genetic] sequencing and looking for variants,\u201d Hodcroft says. \u201cAnd that\u2019s fantastic. This is exactly what I\u2019ve been kind of begging for for a long time \u2014 for more countries to really dedicate resources to this.\u201d But with the increased vigilance, she says, \u201cwe\u2019re going to see a lot of false alarm variants.\u201d <\/p>\n But there also might be more variants of concern in the near future, as the virus is about to get hit by another big selection pressure: vaccines. <\/p>\n If, due to random mutations, there\u2019s a strain of the virus that is just a little bit better at evading the immunity provided by vaccines, it could spread. <\/p>\n That\u2019s why these viral evolution experts want vaccination to happen as fast as possible. Just as partial immunity in a single immunocompromised person can act as a selection pressure for evolution, partial immunity in the population at large can as well.<\/p>\n \u201cWhat we don\u2019t want is for there to be high levels of virus circulating and spending a lot of time with a partially vaccinated population,\u201d Hodcroft says. \u201cWe want to keep case numbers while we\u2019re vaccinating as low as we can.\u201d<\/p>\n That\u2019s because \u201conce you vaccinate hundreds of millions of people, the virus is going to be under really quite intense pressure to evolve [immune] escape variants,\u201d Worobey says. Some of these variants, he warns, \u201cmay already be in existence\u201d among the public but have not yet been detected \u2014 or may soon form as the pandemic continues. \u201cAnd those variants, I think, we can expect to sweep up to much higher frequency once vaccination provides this huge selective force.\u201d <\/p>\n Evolution happens when there\u2019s a lot of genetic diversity, which then meets a selection pressure. This is what\u2019s happening as the pandemic continues during a vaccination campaign.<\/p>\n The good news is that, for now, it appears the existing vaccines will still be broadly effective against the variants, and that it\u2019s possible to update the vaccines to account for future changes. But how can we stop more viral evolution from happening in the first place? <\/p>\n \u201cThe best way to avoid it is to go back in time and not allow the pandemic to spin so out of control,\u201d Worobey says. \u201cIf we had done that, and then vaccinated, then we would have been in a much less dangerous situation.\u201d <\/p>\n \n \n \n \n \n \n