No, the COVID-19 virus is not getting more contagious

By Mark Lynas

May 7, 2020

Or at least, there’s no strong evidence for it yet.

You might have seen an avalanche of scary-looking headlines over the past couple of days suggesting that the COVID-19 virus is mutating into more virulent forms.

As reported in the Washington Post, one group of researchers “believes the virus has mutated to become more contagious.” The Los Angeles Times headlined its piece: “Scientists say a now-dominant strain of the coronavirus could be more contagious than original”.

But some extreme caution is in order.

Most importantly, the paper which is referred to in the press coverage — as in fairness all the mainstream media reports are at pains to point out — is a preprint, which means it has not yet been published in a peer-reviewed journal.

This is an important distinction because it means that its methodology has not yet been properly assessed by other experts, and therefore its conclusions can only be seen as tentative at best.

Early on in the pandemic, a preprint paper by Indian scientists seeded the idea that the novel coronavirus resembled HIV and may have therefore been developed in a lab. This sparked numerous conspiracy theories, many of which continue to circulate despite the fact that the offending paper was debunked and rapidly withdrawn.

Hence the caution with preprints.

This new paper is of a higher quality, however, and deserves proper study. The researchers, led by Bette Korber at Los Alamos National Laboratory in the United States, identify mutations in the SARS-CoV-2 virus’s infamous spike protein. One of these mutations, termed D614G, is “increasing in frequency at an alarming rate, indicating a fitness advantage relative to the original Wuhan strain” of COVID-19, the scientists suggest.

Moreover, they write in the paper that they are “concerned that if the D614G mutation can increase transmissibility, it might also impact severity of disease,” and cite data gathered from hospitalized COVID patients in Sheffield, United Kingdom, suggesting that patients carrying the D614 mutation may have had “higher viral loads.”

Lawrence Young, professor of molecular oncology at the University of Warwick, UK (who was not involved in the study), commented: “These are not different strains or types of virus, they are viruses with minor changes and we don’t know if these changes have any clinically meaningful effects.”

Indeed, Korber et al themselves warn that they found “no significant correlation found between D614G status and hospitalization status” with the Sheffield group of COVID patients.

In another recent preprint paper the authors, who are based at the London School of Hygiene & Tropical Medicine (LSHTM), studied the genomes of over 5,300 virus samples from around the world and looked for evidence of “convergent evolution” — mutations which have evolved independently multiple times and therefore might be beneficial to the virus.

This evidence might then suggest that the COVID-19 virus is mutating in ways that may make it more difficult to control with drugs and vaccines, or perhaps make it more virulent.

They also noted the D614G spike protein mutation, writing that it and others “are putatively the result of selection pressure and should be characterized further to understand how the virus is adapting to human transmission.”

Speaking to the Alliance for Science, Professor Martin Hibberd from the LSHTM — a lead author on the new study — said: “In our paper we highlight several mutations that seem to be important to the virus. The virus hasn’t altered due to pressure from drugs as we have not yet developed them so it is most likely due to transmission — but whether that relates to virulence or not we don’t know.”

Hibberd cautioned, however, that “we are mostly getting samples from the most severe patients” in hospitals rather than asymptomatics, who are mostly not tested. This might mean that “we have a little bit of a biased sample so that limits our full interpretation of the data.”

Regarding the D614G mutation specifically, Hibberd told the Alliance: “We’re flagging it up; we think that other scientists should be interested in it. In a worst-case scenario this could be the start of something that would be important.”

Regarding the mutation rate of SARS-CoV-2, Hibberd continued: “It looks like the mutation rate is normal or even below normal. Overall it looks pretty stable, so that’s encouraging. But you only need a few key mutations to change that picture.”

Current analyses based on virus genetic ‘”family trees” suggest that seasonal influenza mutates roughly four times as fast as the COVID-19 virus.

The relatively low mutation rate observed so far should be good news for all of us, not least because it will make vaccination efforts — the only likely long-term solution to the pandemic — more likely to succeed.

So lurid headlines and scary social media memes aside, there is not yet much convincing evidence that the COVID-19 virus is mutating rapidly, or that it is becoming any more transmissible or lethal.

But mutations are happening, and they need to be monitored in case they do impact on transmissibility or virulence. Fortunately, scientific teams around the world are doing just that.