Coronavirus 2.0 may be up to NINE TIMES more contagious … but that may be cause for celebration

Peter Andrews is an Irish science journalist and writer based in London. He has a background in the life sciences, and graduated from the University of Glasgow with a degree in genetics

3 Jul, 2020 16:24 / Updated 2 years ago

A major global study of coronavirus DNA sequences has confirmed that a mutant strain known as Spike D614G is far more contagious than previous strains, but no more lethal.

The news comes from research published this week in the US scientific journal ‘Cell’. It involved the genetic sequencing of more than 6,000 coronavirus DNA sequences collected from around the world. Of all of these thousands of variants, one that had the researchers particularly worried was the Spike D614G strain – a mutant virus with a crucial change in its DNA code affecting the so-called ‘spike proteins’ on the virus’s surface. These spikes are what allow it to enter human cells, and the mutation seems to make it even better at doing so.

A preliminary version of these findings had already been published on the open-access preprint repository bioRxiv ahead of a peer review as “an early warning” to other researchers studying new strains of the virus. But, since then, the scientists behind the study have confirmed that the new strain is not associated with “increased disease severity.” In other words, it doesn’t make people any sicker than the previous strains that initially spread in Europe and America. 

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Champagne, anyone?

So, why is this good news? Isn’t everything we hear from politicians, public-health officials and the mainstream media about how we should slow down, stop and even crush the spread of the virus? They’ve all been singing from the same hymn sheet on this message for months now. But there’s one small problem: they haven’t a clue what they’re talking about.

Again, attention should be drawn here to the fundamental principle that governs the life cycle of a respiratory virus: a successful virus is a mild virus. A host who is severely weakened, or dead, cannot spread the virus through coughs and sneezes. As the virus replicates and evolves, mutations that tend to make it milder (and, therefore, less deadly) will tend to build up in the most prevalent strains.

Thank God this isn’t a different kind of virus, such as Ebola, which can be simultaneously deadly and contagious, because it spreads through bodily fluids. A respiratory virus can be only one or the other, (or somewhere on the spectrum in between).

If you don’t believe me, how about drawing on the expertise of Lawrence Young, a professor of molecular oncology at the University of Warwick. He wasn’t involved with the study, so had no vested interest. He told CNN: “The current work suggests that, while the Spike D614G variant may be more infectious, it is not more pathogenic. There is a hope that as the SARS-CoV-2 infection spreads, the virus might become less pathogenic.”

Or how about Edward Feil, a professor of biology and biochemistry at the University of Bath. Writing in The Spectator on Friday, he explains how predicting the future spread of a virus – even an active one of which the DNA sequence is known – isn’t feasible: “It is near-impossible to predict the future trajectories of virulence and transmissibility of emerging pathogens.” However, he does begin by citing the common wisdom that any competent biology student should know: “a new pathogen […] will evolve over time to grow more benign and live in amity with its host.” That is exactly what Spike D614G represents.

Faster, virus! Spread! Spread!

How sure am I that spreading the virus is actually better for public health than not spreading it? Not 100 percent sure, but a hell of a lot more certain than the politicians and the highly paid civil-service toadies at their heels, so rarely absent from our television screens these days.

As for the second wave of lore, an idea as attractive and unsubstantiated as a unicorn, this news will offer more encouragement to believers. Of course, a more virulent strain could well lead to more cases of the virus – although as President Trump said so wisely the other day: “If we stop testing right now, we’d have very few cases, actually.” This prompted a minor media hissy fit, but Trump was literally right, in the sense that the cases would not be identified.

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If Trump’s not your bag, how about following the lead of Sunetra Gupta, professor of theoretical epidemiology at the University of Oxford, and a lead author of the ‘Oxford model’. This was a prescient and sensible alternative to Neil Ferguson’s Imperial College London model on Covid-19, which predicted half a million UK deaths. The Oxford model accounted for the fact that the virus may have spread freely throughout the population before lockdowns were imposed, thus rendering them pointless. 

According to Professor Gupta, deaths, and not cases, are “the only reliable measure.” And, if there is a second wave in deaths, I’ll start believing in unicorns.

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