The New Zealand Herald

Why the rapid spread of the mutant virus could be cause for hope

- Sarah Newey

What does it mean when a virus mutates? It’s a question that has become particular­ly pertinent as the threat of a new Sars-Cov-2 variant has wreaked havoc in Britain and beyond.

B.1.1.7 — also known as VUI202012/01 (the first “variant under investigat­ion” in December) — is far from the first change detected in the coronaviru­s. There were more than 12,000 mutations detected in the first 50,000 Sars-Cov-2 genomes studied and scientists have now recorded more than four times that number.

Most of these mutations have little impact. They are akin to misspellin­g a word, the letters are jumbled but the meaning remains the same. But occasional­ly, a mutation will trigger a change of behaviour in a virus.

This is the case with B.1.1.7. Nervtag, a sub-committee of the UK’s Sage scientific advisory group, has said it is “highly confident” the new variant appears to increase the ability of the virus to infect cells. They are also concerned that it is rapidly replacing other versions of the virus.

For some, the increased transmissi­bility could hide some positives.

“The general rule in virology is that better transmissi­on is associated with milder illness,” says Ian Jones, a professor of virology at the University of Reading. “So even if transmissi­on is higher the virus may be less dangerous.”

If a virus mutates to become more deadly it is likely to kill those it infects before it can jump to other people. Patients with Ebola rapidly develop symptoms and it has a very high death rate, reducing its spread.

Professor Jones points to analysis of avian flu in the lab as a good example. “[Experiment­s] are notorious for showing that H5 [avian influenza virus] could become transmissi­ble, but when that happened the virus did not kill any of the animals used,” he says.

In short, the virus was either lethal or very infectious.

The 1918 Spanish flu pandemic appears to prove this point.

It is thought, but not proven, that the second wave was more deadly because of a change in the H1N1 virus.

By 1920 the virus had evolved to become less lethal — now it causes seasonal flu.

Yet other scientists are sceptical. “It’s not always true,” says Jonathan Ball, a professor of virology at the University of Nottingham. “Evolution can favour a virus that can persist and transmit more.” Rabies, for instance, spreads because of the aggressive disease it triggers.

So what does this mean for SarsCov-2? Experts are split about whether the virus is likely to mutate to become more — or less — deadly. But they all insist we should not give the virus the space to find out.

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