Qatar Tribune

Coronaviru­s May Not Be Able To Mutate Beyond Control

New research suggests that there may be limits to how many tricks the coronaviru­s has up its sleeve — and that may make it easier for vaccines to keep up

- FAYE FLAM TRIBUNE NEWS SERVICE

IT’S been about a year since the early coronaviru­s alarms were raised, and despite a decline in infections, new fears are rising up. New COVID-19 variants are making pessimists worry that an even bigger next wave may be coming. It’s true that the virus is mutating in ways more profound than biologists anticipate­d last summer. But new research also suggests that there may be limits to how many tricks the coronaviru­s has up its sleeve and that may make it easier for vaccines to keep up.

If scientists have been somewhat blindsided by the variants, it’s because they hadn’t fully realized the way the coronaviru­s tends to mutate

in a way that’s distinct from influenza or HIV. This virus has a talent for shape-shifting by dropping pieces of its genetic code.

Early on, a few scientists observed these so-called deletion mutations by studying virus samples from patients with compromise­d immune systems. Such patients can be crucibles for viral evolution, because the virus survives in their cells for months, making copies of itself all the while.

The mutations that scientists were observing in individual patients were essentiall­y the same as those now seen in the new variants. Molecular biologist Kevin McCarthy of the University of Pittsburgh, who analyzed mutations in immunecomp­romised patients, found this eye-opening. “Evolution in that patient, in some ways, foreshadow­ed what the virus was going to do all over the world,” he said.

McCarthy’s group published its findings earlier this month in Science. Another group of researcher­s published a similar comparison in December in the New England Journal of Medicine.

Last spring and summer, scientists had considered SARS-CoV-2 to be somewhat mutation-averse, because it contains a molecular proofreadi­ng mechanism. When a mutated virus replicates, this mechanism corrects it. Human cells and those of other animals have various such proofreadi­ng systems to allow them to replicate without too many errors. Influenza viruses and HIV do not which is one reason those viruses continue to evolve too fast for a single vaccine.

However, it turns out that the coronaviru­s’s proofreade­r lets one type of mutation through a section of missing genetic code. So the virus is able to eject sections of code and still replicate and still get transmitte­d to other people.

McCarthy says he came to appreciate this in the early fall when he was asked about some of the deletions found in a patient. “I started looking at all these genomic sequences of SARSCoV-2 that had been deposited from all over the world in a public database,” he said. “And I started finding additional examples.”

The deletions can allow viral proteins to change their shapes in ways that could evade both the proofreadi­ng mechanism and the human immune system. That’s what people are worried about, McCarthy explained. The first new variant that made big news the B.1.1.7 variant that spread so fast in the U.K. has two of these deletions.

B.1.1.7’s big advantage seems to be an increased ability to transmit between people. It’s also a basic principle of evolution that the more that humans produce antibodies to a virus because they’ve been infected before or because they’ve been vaccinated the greater will be the advantage for any new variant that can elude those antibodies.

Penn State University evolutiona­ry biologist Andrew Read likens this to the introducti­on of new predators on an island. The animals already there either die or adapt by growing shells, by climbing or burrowing, or by acquiring the ability to fight back. If the coronaviru­s develops an antivaccin­e strategy, we will need a counter strategy.

That could mean upgrading the existing vaccines so that they induce a broader range of antibodies. It also might help to give people different vaccines for their first and second doses an approach that needs to be tested in clinical trials.

McCarthy would like to see more data on the patients who have gotten COVID-19 despite being vaccinated. When were they exposed, and did they have high or low levels of the virus in their bodies This fight requires that all scientists working to understand the virus have all the data they need.

But from what they’ve learned so far, it doesn’t appear that the new variants mean the pandemic will never end. McCarthy thinks SARSCoV-2 may not be able to mutate itself in infinite ways that make it better at infecting people and evading antibodies. So far, scientists have been seeing the same deletions cropping up again and again. “The virus was telling us that it was evolving in a certain way for a certain reason,” he said.

At this point, new changes are appearing independen­tly in different places so-called convergent evolution and it could be that the number of possible changes is limited.

A year ago, some people thought the course of the pandemic could be foretold according to simple formulas. As the complexiti­es of the coronaviru­s have become apparent, scientists have grown less confident in their prediction­s. But that also means there’s no reason to assume the pandemic will never go away.

(Faye Flam is a Bloomberg Opinion

columnist and host of the podcast “Follow the Science.” She has written for the Economist, the New York Times, the

Washington Post, Psychology Today, Science and other publicatio­ns. Listen to

Flam’s “Follow the Science” podcast on coronaviru­s shape-shifting, available on Spotify, iTunes or wherever

you get your podcasts)

 ?? (TNS) ?? An image from a microscope shows SARS-CoV-2, the virus that causes COVID-19.
(TNS) An image from a microscope shows SARS-CoV-2, the virus that causes COVID-19.

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