Scientists trace more contagious COVID-19 mutation to see how it dominated the world

Several times since the coronavirus pandemic began, scientists from around the world announced that they’ve discovered new mutations in the virus’ genetic material, sending shivers down the spines of a scared yet confused public.

The term “mutation” often has a negative connotation, but the action it carries helps scientists study where a pathogen came from and how it has been spreading, ultimately teaching experts how to contain it.

These minute changes in the coronavirus’ genome are normal and indeed happening, but most are insignificant and don’t change how deadly or infectious it is.

Now, new research adds to several previous papers that also say the coronavirus has diverged in two: the second, more dominant one carrying a mutation termed D614G that appears to have made it more contagious ⁠— at least in a laboratory setting.

What scientists don’t know is whether the discovered mutation affects symptom severity or increases mortality.

“[Mutations] are not predictable and I don’t think there’s any real pinpointing of what specifically is going to be the catalyst for [change]. It just reacts to its environment,” Dr. Andria Rusk, an assistant professor specializing in infectious disease at Florida International University’s College of Public Health and Social Work, told McClatchy News.

The first version of SARS-CoV-2 came from Wuhan, China⁠ — where the disease first emerged.

But as scientists feverishly sequenced hundreds of viral samples from infected patients, they learned a second version developed just before Europe started experiencing a plethora of cases unseen anywhere else.

Experts say it’s unknown how the virus was introduced to Europe, but what they do know is that travelers from the continent entering the U.S. brought the new strain over, which spread undetected for weeks before America shut down, genetic sequences revealed, according to The New York Times.

Now this newer version containing the D614G mutation is the main type ravaging the world.

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It’s important to understand that not every mutation will lead to a new strain or version of coronavirus, infectious disease expert Dr. Nathan Grubaugh at Yale School of Medicine told The Atlantic.

“Think about dog breeds as equivalents of strains: A corgi is clearly different from a Great Dane, but a black-haired corgi is functionally the same as a brown-haired one, and wouldn’t count as a separate breed,” author Ed Yong wrote in the article.

In April, Chinese researchers said the coronavirus had already mutated into more than 30 different strains, according to their study published in the preprint server medRxiv.

The group claimed one of the new strains — the version with the D614G mutation — was more infectious.

Since then, there have been at least a dozen papers calling out the dominant “G variant” that now resides in the bodies of more than 11.9 million people worldwide.

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Lab studies show this mutated form of the virus is 10 times more infectious than the original version from Wuhan, China, Scripps Research virologist Dr. Hyeryun Choe, senior author of an unpublished study on the newer strain, told The Washington Post.

This is because the outer membrane of the older version (D614) isn’t stable and breaks apart easily, making it harder for it to enter human cells.

But the new strain has “four to five times” more spikes on the virus’ surface that allow it to stay intact and infect cells more easily, Choe said in a Scripps news release.

A separate study on the variant recently was published in the journal Cell. The paper also suggests the new strain is more contagious because patients with the G variant have more of the virus in their bodies, making them more likely to spread it to others.

The good news is that the new strain does not appear to lead to worse outcomes or increased symptom severity, the Scripps study said.

Does human behavior affect mutation rate?

The idea that mutations are mostly harmless and cause no change in infectiousness seems to be at odds with the discovery of D614G, which may lead many to wonder why the coronavirus “so quickly overwhelmed” Italy and New York unlike it did San Francisco and Washington at the beginning of the year, the Scripps researchers said.

“This virus isn’t going to [change] because people are or are not wearing masks or because countries are open to international travel or closed, but rather the more times a virus moves between different hosts,” Rusk told McClatchy News.

It’s like making a photocopy of your driver’s license, then making a photocopy of the photocopy, Rusk said, “it just corrodes every single time.”

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So while the fate of mutations lies in the virus’ behavior and not ours, it’s comforting to know that SARS-CoV-2 mutates slowly and at a tenth of the speed of influenza, the virus that causes the seasonal flu, The Atlantic reported. This is why the flu vaccine must be updated every year.

Rusk said most of our understanding on viruses made up of RNA-based genetic material such as SARS-CoV-2 are based on what we know about the flu, also an RNA virus.

But the current coronavirus behaves differently than many viruses to date, so comparing the two is not effective.

“It’s kind of like studying bald eagles your entire life and thinking you know everything about birds; that just doesn’t quite make a lot of sense,” she said.