(Bloomberg Opinion) -- In looking at how a tiny virus can bring the world to its knees, one need only look to the power of Darwinian evolution. All living things can evolve, but the virus can evolve a lot faster — in days rather than centuries.
Evolution won’t necessarily favor forms of the virus that are more deadly, or cause more severe illness — the virus gets no benefit from our deaths. But evolution does favor viruses that are more contagious. A previous mutation seems to have increased the transmissibility of the virus in Europe early in 2020, and that’s the version that ran rampant across the U.S. last year. Now there are at least two new variants, both apparently more transmissible still — one discovered in South Africa and another that’s fast expanding outward from the UK. It’s already been found at least three U.S. states and 33 countries.
So far, scientists reassure us, it’s likely our vaccines will work against them, but that could change with the next evolutionary turn. All the more reason to speed up the sluggish pace of vaccination.
That’s because how much more the virus evolves depends on how far it spreads. “The larger the population of individuals who are infected … the more likely it is for the virus to display mutations. It’s a simple numbers game,” says Purdue University virologist David Sanders.
Evolution works through two parts. Organisms build up random mutations, and then natural selection favors those mutants that are more likely to survive and reproduce. The more viral infections people get, the more mutations natural selection has to work with. An out-of-control outbreak gives the virus a Darwinian edge.
Overall, SARS-Cov-2 is relatively slow to accumulate mutations, which usually occur at a steady rate. That’s one reason it’s been possible to discover an effective vaccine. But the new UK variant, dubbed B.1.1.7, isn’t fitting the pattern.
When scientists first identified it in the UK last September, they saw it had 23 mutations — about 20 more than they would have expected, says Harvard epidemiologist William Hanage. Many were so-called nonsynonymous mutations, which means they change the actual proteins that make up the virus and do the work of invading cells and reproducing.(1)
By late November, Hanage says, scientists found that same group of mutations in virus samples from 117 people clustered around Kent.
Some of the mutations in this new variant can show up in the standard PCR test people use to tell if they have the virus. That’s because some of the mutations consist of missing pieces of genetic material — called deletions — and so the PCR tests will register positive for some parts of the virus and negative for others.
“All you need to do is look at the test results and start asking people, so, how many test results are you getting which look weird like this?” he says. That’s what’s allowing scientists to track the rapid spread of this new variant.
Hanage says it’s possible new variants are spreading fast by chance — through a handful of unlucky super-spreader events, for example — but that several lines of evidence suggest there’s more going on. He says he’s impressed by a still-unpublished paper out of the London School of Hygiene and Tropical Medicine, which used patterns in the spread of B.1.1.7 to argue the most likely scenario is that the virus is more contagious.
The types of mutations also suggest greater transmissibility. Ralph Baric, a virologist at the University of North Carolina, says there are mutations in a part of the RNA that influences how many copies the virus can make of itself — the so-called polymerase. That could increase the amount of virus people carry in their upper respiratory tracts, he says, which could make the virus more contagious. There are also mutations in the so-called spike protein, which could improve the ability of the virus to latch onto and invade our cells.
Baric did work in hamsters to make a strong case that the earlier European mutation — sometimes called D to G — made the virus more transmissible. Similar experiments might shed light on the newer variants.
One of the exact same spike protein mutations has also been seen in the new variant that’s spreading in South Africa, says Hanage. That could be a phenomenon known as convergent evolution — independent inventions of the same trait.
The good news is that Baric and Hanage are still optimistic that the approved vaccines will work against these variants. UNC’s Baric says the vaccines induce a number of antibodies that attack different parts of the viral spike protein, so there’s some redundancy built in even if a new variant is somewhat more resistant.
Once vaccines is widely distributed, it’s always possible the virus could evolve to evade it. “That's just the nature of the beast when it comes to infectious disease,” says Hanage. But once fewer people are getting infected, we’ll also be giving the virus far, far fewer chances to mutate — and as few chances as possible to get the upper hand.
The bottom line? We need to get that vaccine out fast.
(1) There was some concern that infected minks in Denmark had something to do with this, since a virus can accumulate mutations faster if it jumps back and forth from a different animal host. Hanage says he doesn’t suspect this mutation is connected to minks, but probably arose in an immune-compromised human who might have hosted an unusually large number of copies of the virus for an unusually long period of time.
This column does not necessarily reflect the opinion of the editorial board or Bloomberg LP and its owners.
Faye Flam is a Bloomberg Opinion columnist. She has written for the Economist, the New York Times, the Washington Post, Psychology Today, Science and other publications. She has a degree in geophysics from the California Institute of Technology.
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