Coronavirus Mutation Helped The Disease Spread, But It Could Be Its Downfall

A watercolor painting showing a coronavirus entering the lungs, surrounded by mucus secreted by respiratory cells, secreted antibodies, and several small immune systems proteins. David S. Goodsel (CC-BY-4.0)

Scientists have shown that SARS-CoV-2, the virus that causes Covid-19, has mutated in a way that’s helped it to spread rapidly around the world. But the mutation isn’t all bad news; it’s also caused a change to the spike protein that makes the virus more vulnerable to vaccines. 

Reporting their findings in the journal Science, scientists at the University of North Carolina at Chapel Hill and the University of Wisconsin-Madison detail a newly identified variant of coronavirus called D614G.

Researchers have known about this variant for several months, with previous research showing it likely emerged in Europe before becoming the most common variant in the world. This new study backs up this idea, suggesting the D614G variant replicates faster and is more transmissible than the virus that originated in China.

To better understand this variant, hamsters were infected with either the newly identified variant or the older ancestral strain, then placed into cages next to eight uninfected hamsters. Air could pass between the cages, but the hamster could not physically touch each other. The experiments suggested that the variant appears to replicate about 10 times faster and is notably more infectious. 

“We saw that the mutant virus transmits better airborne than the [original] virus, which may explain why this virus dominated in humans,” Yoshihiro Kawaoka, study author and virologists at the University of Wisconsin-Madison, said in a statement.

"The D614G virus outcompetes and outgrows the ancestral strain by about 10-fold and replicates extremely efficiently in primary nasal epithelial cells, which are a potentially important site for person-to-person transmission," added Ralph Baric, professor of epidemiology at the UNC-Chapel Hill Gillings School of Global Public Health and professor of microbiology and immunology at the UNC School of Medicine.

It appears that the variant's potency lies in the changes that occurred to its spike protein, the surface protein used by the virus to bind and invade host cells. The D614G mutation was found to have “a flap” on the tip of one spike, which allowed it to become even more effective at binding with cells.

However, this newly acquired strength might also be its downfall. The researchers argue that this flap also means it’s easier for antibodies, such as the ones prompted by a potential vaccine, to disable the virus.

This also suggests why the mutant virus is more infectious but doesn’t necessarily cause a significantly worse illness. As previous research has shown, the D614G is more efficient at getting into cells and more transmissible, but there is  "no significant correlation" between people infected with the variant and their risk of hospitalization. 

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