COVID-19: The coronavirus is mutating, and so far

Coronavirus Covid

A transmission electron micrograph of SARS-CoV-2 virus particles, isolated from a patient, captured and enhanced with color at the Integrated Research Center of the National Institute of Allergy and Infectious Diseases in Fort Detrick, Maryland, USA United.
Image Credit: AFP

You’ve no doubt read recent headlines about patients who have recovered from COVID-19 only to be re-infected with SARS-CoV-2 later – supposedly with a different “strain” of the virus.

At the end of August, information was communicated regarding the world’s first ‘documented’ or ‘confirmed’ case of reinfection with SARS-CoV-2: a man from Hong Kong, diagnosed in March, had contracted ” a new virus ”circulating in Western Europe this summer. The next day, news broke that two people in Europe also appeared to have been re-infected.

After that, it was about stories about the first American case of its kind – involving a patient from Nevada who allegedly suffered worse symptoms the second time around. The pre-printed (non-peer reviewed) study on which these reports were based no longer appears to be available.

All this talk about new, perhaps more virulent, forms of SARS-CoV-2 is unnecessarily creating fear and confusion.

Evidence and science

On the one hand, isolated cases of reinfection also occur with other viruses. This fact is not necessarily alarming. Reinfection usually only tells us how the human immune system is working. This is not, at first glance, proof that a virus has mutated in a way that makes it more dangerous.

On the other hand, viruses mutate regularly – and most of these changes are bad for the virus or even fatal, according to some studies. (A minority of mutations are neutral, and only a small minority are beneficial.) The word “mutation” may sound worrisome, but it is a trivial fact of viral life and its implications are most often not harmful to humans.

And yes, SARS-CoV-2 is also mutating. So what?

The real question is, has it become more virulent or more infectious than it was when it was first detected in Wuhan, central China, in December? The evidence suggests that it is not.

The slow rate of mutation of the coronavirus is good news for us: a virus that has evolved faster would be more likely to outperform any vaccines or drugs developed to counter it.

Like the viruses that give us the flu or measles, SARS-CoV-2 has a genetic code made up of RNA, or ribonucleic acid. But RNA is highly mutable, and as SARS-CoV-2 infects us by using our body’s cells to replicate over and over again, every time its genome is copied, an error can creep in.

Most mutations are lost quickly, either by chance or because they damage some of the virus’s main functions. Only a small proportion ends up spreading widely or lasting. Mutation can be the fuel of evolution, but, especially for an RNA virus, it is also the status quo.

RNA viruses tend to evolve quickly – about a million times faster than human genes. However, if SARS-CoV-2 stands out among them, it is to evolve more slowly than many: about five times slower than influenza viruses, for example.

SARS-CoV-2 is on the slow path of evolution

According to Nextstrain, an open-source project that tracks the evolution of pathogens in real time, and other sources, SARS-CoV-2 accumulates on average about two mutations per month – which means that the forms of the virus that circulate today are only about 15 different mutations of the first version attributed to the Wuhan epidemic.

This is a tiny number given that the SARS-CoV-2 genome is about 30,000 nucleotides long. And that also means that today’s versions of the virus are roughly 99.95% identical to the Wuhan original. For an RNA virus, SARS-CoV-2 is slow growing.

(So ​​to speak of SARS-CoV-2 which has developed into so many different “strains” is misleading. Scientists tend to reserve the word for versions of a virus that differ in major biological ways. forms of SARS-CoV-2 are very similar; better to call them “variants”.)

The slow rate of mutation of the coronavirus is good news for us: a virus that has evolved faster would be more likely to outperform any vaccines or drugs developed to counter it.

Having said that, have even small mutations so far changed SARS-CoV-2 in significant ways?

For example, has it become more deadly?

To my knowledge, there is no evidence to date that SARS-CoV-2 has become more virulent or more deadly – nor, for that matter, that it is less so.

For example, a recent (not yet peer-reviewed) pre-print article by Erik Volz, Imperial College London Medical School, and many colleagues from other institutions – including members of COVID -19 Genomics UK Consortium – which analyzed 25,000 SARS-CoV-2 whole genome sequences collected in the UK revealed that a particular mutation in the virus, known as D614G, did not increase mortality in patients.

Which D614G mutation?

There has been a lot of discussion about whether the D614G mutation – which affects the virus’s so-called spike protein – has made SARS-CoV-2 more infectious.
The spike protein is found on the surface of the coronavirus, and this is important because it is the part of the virus that attaches itself to the host’s cells. “D614G” is a shorthand for a change at position 614 of the spike protein, from an aspartic acid (D) to an amino acid glycine (G). (The technical documentation refers to “D614” as a previous configuration and “G614” as a subsequent configuration.)
The D614G mutation, which probably first appeared in China, appeared to become increasingly common during the outbreak in northern Italy in February. The G614 form of the virus has since spread around the world and has become the dominant variant.

The D614G mutation appears to have increased the infectivity of the coronavirus – at least in cells grown in the lab, according to a recent article by computer biologist Bette Korber and others published in the journal Cell.

Apparently, based in part on this study and others, health authorities in various countries have claimed that the G614 form of the coronavirus may be 10 times more infectious than the version first detected in Wuhan.

But as some epidemiologists have warned, it’s difficult, if not reckless, to extrapolate from lab results to explain how the virus actually spreads in an actual population.

Whether SARS-CoV-2 is becoming increasingly infectious or fatal is an important question, especially since it does not appear that this virus will be eradicated anytime soon.

I don’t think the evolution of SARS-CoV-2 is the cause of the continued spread of the virus. The coronavirus remains good for spreading because most of us are still susceptible to it; we are not immune, and it can still find new hosts to infect relatively easily.

In the same issue of Cell that published the Korber article, viral epidemiologist Nathan Grubaugh and colleagues argued that “the increase in the frequency of G614 could be explained by chance and the epidemiology of the pandemic. “.

In other words: the next time you compare different outbreaks and start wondering or worrying about the variations, first assume that those variations are related to conditions on the ground, rather than to anything. or concerning the virus itself, as a new mutation.

How variants affect death rates

Take, for example, the wave of SARS-CoV-2 infections that has hit Australia since June. Although there has been a major outbreak in the state of Victoria (peaking at around 700 cases per day), that in the state of New South Wales has been minor so far (with a number of cases daily usually around 10) – but both were caused by the same variant of the coronavirus, the one with the D614G mutation.

The precise reasons for these differences are still being investigated, but it can simply be said that because the outbreak hit Victoria first, NSW health officials have had more time to prepare.

Death rates also differ from place to place, and in some places the virus can appear to kill more people. But again, these variations probably say less about the virus than it does about the differences in how the disease is treated, or where the virus has spread primarily among vulnerable populations, such as people living in rural areas. retirement homes.

Moreover, even if the D614G mutation increases the infectivity of the virus in humans, this fact probably does not have major implications for our prospects for the development of an effective vaccine. The mutation affects the spike protein, but not the part of it that neutralizing antibodies in the human immune system target when the body is defending itself against infection.

Viruses are constantly mutating; SARS-CoV-2 is no different. And it is essential that we continue to monitor when and how, and with what effects, it is evolving.

Whether SARS-CoV-2 is becoming increasingly infectious or fatal is an important question, especially since it does not appear that this virus will be eradicated any time soon. More likely, it will become an endemic pathogen in humans, as daily as the flu.

For now, however, SARS-CoV-2 is essentially the same virus that emerged in December. Sure, it has mutated, but not, so far, in a way that should change the way scientists think about dealing with it – not in a way that you should worry about.

– Edward Holmes is an evolutionary virologist at the University of Sydney, Australia

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