UPDATE: Pennsylvania officials said Thursday that the new virus variant has been identified in a state resident who traveled internationally. Scientists now are in general agreement that the new virus variant spreads more easily, though by how much remains unclear, and they say it does not appear to make people sicker.
As if 2020 needed any more alarming headlines, each day brings news about the new “mutant” strain of the coronavirus identified in Britain, where health officials have proclaimed that it spreads far more readily than the microbe that has been crisscrossing the globe for months.
Scientists who study the biology of viruses say that so far, there is no proof that this new strain is more transmissible, only what amounts to circumstantial evidence. Human behavior and random chance also could explain the sudden emergence of the strain which, given that it was identified in a Colorado man this week, likely is already widespread in the United States.
And even if the new strain turns out to spread more easily, there is no indication that it makes people more sick or that it has changed anywhere near enough that the vaccines will not work.
We spoke with three researchers for a crash course in Viral Mutation 101: Susan R. Weiss at the University of Pennsylvania, Zachary Klase of Drexel University, and Glenn F. Rall at Fox Chase Cancer Center.
The bottom line: Are you wearing masks and limiting the amount of time spent in crowded, indoor spaces? Good, Weiss said. Keep it up.
“We should be doing the same things that we should already be doing anyway,” she said.
The genetic code of the coronavirus is close to 30,000 letters long. Every time it penetrates a human cell, using that code to make thousands of copies of itself, a few mistakes are made — on average, two or three with each new copy. Some of these random errors may hamper the microbe’s ability to spread to other cells, and ultimately to other people. Many of the mistakes will have no effect. A very few might enable it to spread more easily.
It comes down to that Darwinian notion often simplified as “survival of the fittest.” Versions of the virus that are easily transmitted are the ones that stick around. But the coronavirus has been spreading readily since the beginning, so there is little evolutionary pressure for it to change much, said Klase, an associate professor of pharmacology at Drexel’s College of Medicine.
Rall, who coauthored Principles of Virology, a standard text in the field, likened the process to a young pianist learning to play a Beethoven sonata. Some attempts will be so bad that the student has to stop and start over. Other attempts will have mistakes, but the piece is recognizable.
“Rarely,” Rall said, “you might imagine that he or she incorporates something that makes the piece sound better than the original.”
In early December, the number of people with COVID-19 surged in Kent, in southeastern England. The cases were identified in the usual way, with nasal swabs and a PCR test. That test is used to look for three telltale regions of the viral genetic code. While these regions consist of just hundreds of “letters” out of the 30,000-letter blueprint, this sample is good enough to make the ID.
But to get a better idea of what was happening in Kent, British scientists sequenced the entire 30,000-letter code for a sample of the patients. It turned out the virus had acquired a set of 23 mutations, including some misspellings and two short sections that were simply deleted.
Those deleted areas occurred in the section of genetic code that holds the recipe for the spike protein: the little protrusions on the surface of each virus particle.
By chance, those deletions fell in one of the three regions that are used in the PCR tests. That meant England and the rest of the world could quickly identify more cases of the new variant without the lengthier process of sequencing the entire viral genetic code. All it takes is a standard PCR test, and if the person tests positive for two of the signature regions but not the third, bingo.
The new strain seems to have spread rapidly, but that might not be the result of the virus itself. It could simply be that someone who was infected with that strain engaged in “super-spreader” behavior, perhaps spending hours at a crowded British pub.
In other words, a particular virus strain can become dominant through behavior of its human hosts — what infectious-disease experts call a “founder effect.”
British epidemiologists have sought to tease out whether that is the case here, but the evidence so far is murky.
This is where it gets tricky. PCR tests work by “amplifying” the genetic material in a sample until there is enough to be detected. The more amplification cycles that are needed to reach that threshold, the less genetic material was present at the beginning.
For the Kent samples, the PCR testing machines needed fewer cycles than average to get a detectable level of genetic material, suggesting that the patients’ nasal passages contained more to begin with.
That could mean their airways contained more virus, but not necessarily. The test measures only genetic material, not the virus itself. A true test of a person’s “viral load” requires sophisticated lab experiments.
And even if the patients had higher viral loads, that does not mean they would be more likely to spread it. Proof would require direct measurement of transmission in live human experiments, which would never be done with such a dangerous virus.
Several of the mutations in the new strain seem as if they might improve the “fitness” of the coronavirus, said Weiss, a professor of microbiology at Penn’s Perelman School of Medicine. But the jury is still out.
We’ve been told from the beginning that COVID is not like the flu, in the sense that it is more likely to cause severe and long-lasting consequences. But in one respect, the coronavirus is cutting us a break: vaccines.
The flu is a “segmented” virus, meaning that in addition to mutating a few letters at a time like any virus, it also can swap entire segments with its peers, like kids trading baseball cards. That’s why each year, health officials must try to predict which combination of flu segments is likely to predominate, so that drug companies can tweak their vaccines accordingly.
Coronaviruses are not segmented, so the only issue is mutation. It is true that this virus could eventually mutate enough to escape the protection from the vaccines, but the number of mutations so far represents well under 1% of the total 30,000-letter blueprint.
Traditional vaccines work by exposing recipients to a weakened or inactivated form of an entire virus, so their immune systems can learn to fight back in the event of a real infection. The Moderna and Pfizer-BioNTech vaccines, on the other hand, work by coaxing recipients to make just a fragment of the virus — the spike protein — so the immune system can respond with customized antibodies and other defenses. Several of the mutations in the new virus variant happen to occur in the spike, but just one is thought to possibly affect the ability of antibodies to recognize the virus.
In people who receive the vaccine, the immune system learns to target 20 regions of the spike. So even if the one mutation impairs recognition by antibodies — and that remains unproven — 19 more are still good.
Rall, the Fox Chase virologist, likened the spike protein to a crumpled piece of paper.
“The antibodies are binding to little nooks and crannies on that,” he said. With the mutation, “you’ve maybe just snipped off a little piece of one corner of the piece of paper. But in essence, the ball of paper still looks the same.”
Staff writer Marie McCullough contributed to this article.