As if 2020 needed any more alarming headlines, each day brings news about the new “mutant” strain of the coronavirus identified in Great Britain, where health officials have proclaimed that it spreads far more readily than the microbe that has been crisscrossing the globe for months.
Well, maybe.
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 U.S.
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.
Question: What causes mutations?
Answer: 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 get passed on to other cells, and ultimately to other people. Many of the mistakes will have no effect at all. 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.”
Q: How’d they find the new strain?
A: In early December, the number of people with COVID surged in Kent, in southeastern England. The cases were identified in the usual way, with nasal swabs and a test abbreviated as PCR. That test identifies the presence or absence of three telltale regions of the viral genetic code. While these regions consist of just hundreds of “letters” out of the 30,000-letter genetic code, 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.
But genetic sequencing requires specialized equipment. How’d they find this strain in thousands of others?
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 that form its namesake corona.
By chance, those deletions fell in one of the three regions that are used in the PCR tests. That meant that 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.
Q: Why the doubt about whether the virus is more transmissible?
A: 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 unwise “super-spreader” behavior, perhaps spending hours at a British pub with dozens of others nearby.
In other words, a particular strain of a virus can quickly 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, comparing various characteristics of people infected with the new and old strains, but the evidence so far is murky.
Q: So how would they make the case?
A: 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 samples taken from the Kent patients, the PCR testing machines needed fewer cycles than average to get a detectable level 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,” on the other hand, requires sophisticated experiments in a laboratory.
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. The most that might happen is experiments in lab animals.
