Coronavirus strain D614G is ‘better at infecting human cells’ than original version

A mutated version of the coronavirus, dubbed D614G, is found in 85% of cases worldwide and researchers believe this version is so common because its genetic modification makes it more infectious and better at spreading.

However, an expert analysis from the University of North Carolina found that the change did not make it more deadly or likely to cause severe symptoms.

D614G is by far the most common strain of coronavirus in humans worldwide and first appeared in February in Europe.

International travel allowed this variant to spread across the continent and into the Americas, Oceania, and Asia in a matter of weeks.

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In the early days of the Covid-19 pandemic, the dominant form of the virus was a variant now referred to as “D strain”.

However, the D614G mutation appeared at a specific location, position 614, on the virus spike protein, in a European patient.

This viral spike hijacks the human ACE2 receptor and thus infects human cells.

The location of the mutation is at a critical time that affects how the virus divides into two after infiltrating a cell.

The mutation is very small and simple, an amino acid changes from a D (aspartate) to a G (glycine), hence the nickname D614G.

As Italians, Brits and others from coronavirus hotspots traveled to Asia, Australia and America, the D614G virus subsequently took hold in those regions.

Data from a study published last month shows a peak in the G strain in Europe in early February, followed by another resurgence of the G variant fifteen days later.

In early March, cases of D614G were spotted around the world, and this specific mutation accounted for about a quarter of all cases.

It continued to take over and made up more than 70% of all cases in May, and the number is now estimated to exceed 85%.

Scientists tried to determine why the D614G strain emerged as the main form of SARS-CoV-2, the virus that causes Covid-19.

The latest study, published in the journal Science, created a lab-built version of the mutant virus and observed how it infected mice and hamsters modified to have the human version of the ACE2 receptor.

ACE2 has been dubbed the ‘gateway to the cell’ for the coronavirus and the interaction between it and the viral peak is the focus of much research.

Yixuan Hou, lead author of the study, at the University of North Carolina, says the amount of virus an animal was infected with was similar whether it was strain D or G.

“However, the D614G variant transmits much faster and has shown better competitive ability than the wild type virus in hamsters.

“These data show that the D614G substitution improves SARS-CoV-2 infectivity, competitiveness, and transmission in primary human cells and animal models.

Hamsters with the mutated strain lost somewhat more weight than those with the original variant but the authors say this is negligible and overall the D614G substitution does not significantly improve the pathogenesis of the virus.

The variant was transmitted much faster in hamsters, which the authors say indicates that the virus evolved not for greater pathogenicity, but for better human transmissibility.

These findings, although not in humans, offer some of the most convincing evidence to date that the mutation spread rapidly due to improved transmissibility.

The researchers also used human cells from gates to see if the mutated strain was more efficient at infecting the cells and found it to be.

The ancestral version and the mutated version were injected into cells and after three days the G strain was extremely dominant in the cultures.

This happened ‘regardless of the fact that [original] virus was at a 1: 1 or 10: 1 ratio to the isogenic mutant D614G, ”the researchers say.

Although the study confirms that the mutation is more infectious, it cannot be determined why.

However, a recent study, published on the medRxiv preprint server and not yet peer-reviewed, from the University of Louvain in Belgium found that the D614G mutation causes the coronavirus to thrive at 37 ° C, human body temperature.

It is more stable at this temperature than the original D strain, which prefers 33 ° C.

This difference makes the new variant more stable at the exact temperatures seen in the human airways.

The mutation is also associated with an increased ability to manipulate proteases, enzymes in cells that destroy proteins, to facilitate infection.

“ Collectively, our results indicate how the coronavirus spike protein is adapted to the temperature and protease conditions of the airways, to improve virus transmission and pathology, ” the academics write.