Home Health News Has Coronavirus Really Mutated into Two Strains, with One More Transmissible Than The Other? – Newsweek

Has Coronavirus Really Mutated into Two Strains, with One More Transmissible Than The Other? – Newsweek

17 min read

A team of scientists has claimed a more contagious form of the coronavirus which causes COVID-19 has emerged. But as the findings trended online, experts sought to dampen fears that the mutations show a new, more transmissible strain of the virus has emerged, and said there is no evidence to suggest the bug has changed significantly since the pandemic started.

The term “mutation” carries scary connotations of an unusual, substantial change to a virus, which sounds as though it impacts how easily it infects people and how seriously they fall ill.

But mutations are in fact a normal and generally inconsequential part of the life-cycle of these germs.

Viruses are made up of genetic material, called RNA, encased in protein. When they infect a host, like a human, they make new copies of their genetic data in order to replicate. Like kids might make mistakes when noting down information from a chalkboard in class, this process leads to small changes in the virus’ genetic information. These are called mutations. Scientists recently explored how this process has been mischaracterized in pop-culture in a recent article in the journal Nature Microbiology.

Oscar MacLean, a bioinformatician at the Centre for Virus Research at the University of Glasgow, U.K., told Newsweek: “Virus mutations are a guaranteed and unavoidable feature of viral replication, and while it’s important to monitor them, they should not be of concern.” As SARS-CoV-2 (the coronavirus virus which causes COVID-19 disease) continues to spread, having already infected more than 3.7 million people according to Johns Hopkins University, many teams of scientists around the world are doing just that.

Everyone agrees that SARS-CoV-2 is indeed mutating, which isn’t surprising given the above, experts explained to Newsweek. So far, 7,237 mutations have been documented, and just this week, groups at institutions including UCL in the U.K. and Arizona State University published papers on certain tweaks.

But a mutation needs to be very significant for a new strain of SARS-CoV-2 to be declared. Experts told Newsweek that there isn’t evidence of this happening for the bug which causes COVID-19.

MacLean cautioned “We need to be very careful how we describe new ‘types’ of the virus, as these can be overly suggestive terms. By the definition of possessing unique mutations, we would have thousands of ‘strains’ of SARS-CoV-2, however these viruses are all expected to be functionally very similar, and so it’s somewhat meaningless to use this definition.”

Pointing to a study published in the journal Virus Evolution this week which he co-authored, MacLean said there is “no conclusive proof” that the 7,237 mutations have any effect on how SARS-CoV-2 functions.

A motorist rides past a graffiti painted on a road to raise awareness about COVID-19 in Chennai, India, on April 13, 2020.
ARUN SANKAR/AFP via Getty Images

“Most of these mutations are likely to be dead-ends, either occurring in individuals and not being transmitted or in transmission chains which will fizzle out by chance.” Most RNA viruses mutated rapidly, but compared to other “SARS-CoV-2 is actually changing quite slowly,” he said.

The consensus among those studying the virus is that there is only one strain of SARS-CoV-2.

A more transmissible form of SARS-CoV-2?

MacLean‘s said his team’s study casts doubt over claims made in a preliminary paper lead by a team at Los Alamos National Laboratory in California that a mutation to the spike protein which helps the virus invade our cells “is of urgent concern.” The team said their findings, which trended online and prompted debate among scientists, suggested a more contagious form, although not a strain, of SARS-CoV-2 had emerged.

The team submitted their findings to the website bioRxiv, what is known as a pre-print website. That means the findings haven’t been through the rigorous peer review process required to publish in scientific journals. During a fast-moving time like a pandemic, it can be useful to release data in this way to spark debate on a topic.

Drawing from a database where the genetic data from different samples of SARS-CoV-2 from around the world are collected, Bette Korber, a computational biologist at Los Alamos National Laboratory and colleagues, tracked the evolution of its spike protein up until April 13.

“It began spreading in Europe in early February, and when introduced to new regions it rapidly becomes the dominant form,” they wrote.

Variants of the virus with what is called the D614G mutation popped up in Europe February, and in April had become dominant in North America, parts of Europe, and Australia, they said. This form of the virus was different from that which spread out of the original epicenter of the outbreak, the Chinese city of Wuhan, according to the team.

To look at whether the mutation made it more contagious, they assessed genetic data on virus samples collected from patients around the city of Sheffield in the United Kingdom, and found these patients appeared to have higher levels of the virus.

But experts told Newsweek this doesn’t mean there are now two strains of the coronavirus circulating, with one more contagious and threatening than the other.

While the team were right to assess how the virus and its spike protein has mutated, experts who spoke to Newsweek argued the claims about these changing how transmissible the virus were overstated. And just because a mutation is popping up frequently in a population doesn’t necessarily reflect a change in the virus’ function. Their claims based on computational models would need to be verified in lab studies using virus samples, they said.

Jeremy Rossman, honorary senior lecturer in virology at the University of Kent who did not work on the paper, told Newsweek: “Unfortunately, the paper offers a few strongly worded speculations about what the mutation might do, for instance by enabling a person to be infected by a number of types of SARS-CoV-2.

“These are possible outcomes of the mutation, and ones to be investigating and alert for. However, these statements have been picked up on as conclusions coming from the paper, they are only speculations and there is no evidence that this mutation enhances disease or enables co-infection.

“I suspect that the wording of these speculations will be adjusted during the peer-review process to avoid the level of speculation that is currently circulating.”

Rossman argued: “It is important to be very cautious in speculating from these results as there are many possible explanations but without further experiments they are very difficult to prove.

“We are just observing how the virus spreads and what mutations are present; laboratory experiments are needed to see exactly how these mutations are affecting the virus and to determine if they affect virus transmission, replication, disease or immune interactions.”

MacLean gave the example of the viruses which cause Ebola and severe acute respiratory syndrome (SARS). Outbreaks related to specific mutations were assumed to change how the virus behaved “but subsequently were found to not have such effects,” he said.

Addressing the part of the study which looked at patients in the U.K., MacLean said the patients in the two groups weren’t matched according to variables which could affect how severe their illnesses were “so were likely to also have differences unrelated to the virus infecting them, which might confound this result.”

He added: “It’s also unclear how viral load relates to how contagious an infected individual is, which is likely to be driven by many factors.”

Richard Goldstein, professor of pathogen evolution at UCL in the U.K., told Newsweek he finds the analysis “unconvincing” overall. There are many reasons a variant may appear more often than others which has nothing to do with its ability to spread, he said.

For instance, they may appear in locations with high population densities, which lack medical or epidemiological infrastructure, do not practice adequate social distancing, or are transportation hubs.

Other mutations may appear a lot “just due to the random nature of how the infection is spread. Because of these effects, one must be cautious linking increased prevalence with increased transmission rate. In particular, an increase in frequency does not by itself indicate a fitness advantage.”

Goldstein also questioned the team’s approach of supporting their claim with the observation that the mutation is becoming more prevalent in different geographical regions, as they are not isolated from or independent of one another.

“As the COVID-19 pandemic continues to surge, it is important to characterize its behavior—how it is spreading, how fast it is spreading, who is it spreading from, who is it spreading to—as well as changes in this behavior,” Goldstein said. “It is equally important to recognize the limitations in the data, and refrain from making claims that lack adequate support.”

Still, Rossman suggested the hype around certain mutations shouldn’t distract or detract from how important work monitoring them is. Significant mutations could, for instance, affect how antiviral drugs work or vaccines are created, he said.

“Tracking and investigating virus mutations is essential for managing the pandemic,” said Rossman. “While most mutations do not affect the disease, it is possible that some could, this is important to be alert for.”

And as the pandemic of COVID-19, a disease for which we have no specific treatment or vaccine, rages on, the work of scientists including those at the Los Alamos lab are more important than ever.

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