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A mutated coronavirus strain is responsible for most of the world's COVID-19 infections. That doesn't mean it's more dangerous than the original.

May 7, 2020, 04:57 IST
Business Insider
Medical personnel transport a COVID-19 patient to an ICU tent in Cremona, near Milan, Italy.Emanuele Cremaschi/Getty Images
  • Scientists track genetic errors, or mutations, in the coronavirus' genome to study its evolution over time.
  • A preliminary study suggests a mutated coronavirus strain has become dominant worldwide and is therefore more contagious than the original.
  • But not all scientists agree with that conclusion, since there isn't sufficient evidence that the virus' mutations impacted how dangerous it is.
  • It's possible that this dominant form of the virus just "got lucky," one expert said, and seeded major outbreaks in Europe before spreading to the US.
  • Visit Business Insider's homepage for more stories.
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Preliminary research from scientists at Los Alamos National Laboratory suggests that a version of the new coronavirus with a particular mutation is outcompeting all the rest.

The strain is of "urgent concern,"the scientists wrote. "It began spreading in Europe in early February, and when introduced to new regions, it rapidly becomes the dominant form."

Because of this, they suggested, the strain that is now dominant in Europe and North America may be more contagious than the original virus that first spread in China.

It's true that the coronavirus has mutated over time, but many scientists say the mutations noted in the study — which has yet to be peer-reviewed — don't necessarily indicate that the virus has become more dangerous.

"This really isn't easy to show," Emma Hodcroft, a geneticist at the University of Basel in Switzerland who studies the coronavirus' genome, told Business Insider.

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The paper highlights one mutation in the coronavirus' genome

A German scientist works on sequencing the novel coronavirus as part of research into a vaccine.Reuters

The NextStrain project, where Hodcroft is a collaborator, collects samples of the coronavirus from all over the world and sequences their genetic makeup. Researchers then differentiate the samples based on tiny mutations that get introduced into the virus' genetic codes as it replicates and spreads.

These mutations break a virus into separate, trackable strains — a word that geneticists simply use to differentiate samples that aren't identical — whose spread can be mapped over time.

The Los Alamos scientists used computer software to analyze how prevalent certain strains are around the world. They found that versions of the virus with a particular mutation in a part of its genome that determines the shape of its spike-shaped proteins are more prevalent than others.

When the novel coronavirus emerged in China in late 2019, it didn't have that mutation, which scientists have labeled D614G. Geneticists classify the original version as the "D lineage." Strains with the D614G mutation are categorized as the "G lineage" and didn't crop up until February.

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The "G lineage" has become more common over time in Europe, North America, and Australia, according to virologist Trevor Bedford, who works with NextStrain. It seems to have edged out its "D lineage" counterparts, which first dominated in Asia.

The authors of the pre-print study took that trend to mean that the "G lineage" was outcompeting the "D lineage" and that the former must be "a more transmissible form" of the coronavirus. But that's not the only possible explanation.

Two potential explanations for why the "G lineage" is more prevalent

An illustration of the new coronavirus, SARS-CoV-2, which causes the disease COVID-19.CDC

According to the pre-print study, the "G lineage" might be dominating because the mutation makes it more contagious. But the other possible explanation is that the "G lineage" simply got lucky, according to Bedford.

Data shows that the D614G mutation arose just before the virus spread to Europe, so the "G lineage" ended up being the version that spread westward. European outbreaks eventually seeded some outbreaks in the US. But countries in Europe and North America did not enact lockdowns for weeks after their first cases appeared, and some nations were slow to test widely, which allowed the "G lineage" to proliferate.

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Bedford wrote that he "strongly cautions against" assuming that because there is more of the "G lineage" out there, that version virus is better at jumping between people.

Epidemiologist Angie Rasmussen tweeted on Tuesday: "The old adage that correlation does not equal causation applies here. If you are looking at sequence data alone, you can't show effect that this single mutation, spike D614G has on transmission."

Scientists call for more research before worrying about this mutation

Another non-peer-reviewed study published in April suggested that there were at least 30 strains of the coronavirus out there. But even that's not cause for concern, Hodcroft said, since subtle differences between strains don't tend to affect how contagious a particular version of the virus is.

This scanning electron microscope image shows SARS-CoV-2 (round magenta objects) emerging from the surface of cells from a coronavirus patient.NIAID-RML

More research is needed to test whether the Los Alamos scientists' explanation is the right one.

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"Spike D614G may well have functional importance. It may even increase transmissibility," Rasmussen tweeted. "But we won't know until this is tested experimentally."

Hodcroft said experts would need to find a way to remove some of the confounding elements — like the fact that China identified its outbreak and locked down sooner than, say, the US did — in order to better test the Los Alamos hypothesis.

"One thing that would help is if we found a few instances where the two variants of the virus had been introduced to the same place at about the same time, under the same circumstances," Hodcroft told Business Insider.

But even that perfect set-up "still wouldn't prove anything conclusively," she said, adding that experts would be better served by comparing how infectious the two lineages are in lab-grown cells.

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