A Common Mutation May Make New Coronavirus More Vulnerable To Vaccine, Study Says



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Washington, Nov. 13 (PTI) A common mutation in the new coronavirus that has allowed it to spread rapidly around the world may also make it more susceptible to a vaccine, according to a study demonstrating some of the first concrete findings on how SARS- CoV-2, which causes COVID-19, is evolving.

Researchers from the University of North Carolina at Chapel Hill and the University of Wisconsin-Madison in the US noted that the new strain of coronavirus, called D614G, emerged in Europe and has become the most common in the world.

Their study, published in the journal Science, shows that the D614G strain replicates faster and is more transmissible than the virus, originally from China, that spread at the beginning of the pandemic.

While the D614G strain spreads faster, in animal studies it was not associated with more serious disease and the strain is slightly more sensitive to drug neutralization of antibodies, the researchers said.

“ The D614G virus surpasses and exceeds the ancestral strain by approximately 10-fold and replicates extremely efficiently in primary nasal epithelial cells, which are a potentially important site for person-to-person transmission, ” said Ralph Baric, professor at UNC-Chapel Hill.

The researchers believe that the coronavirus strain D614G dominates because it increases the spike protein’s ability to open cells for the virus to enter.

The D614G mutation causes a flap to open at the tip of a spike, allowing the virus to infect cells more efficiently, but also creating a pathway to the vulnerable nucleus of the virus, the researchers said.

With an open flap, it is easier for antibodies, such as those in vaccines currently being tested, to infiltrate and inactivate the virus, they said.

The original spike protein had a ‘D’ at this position, and it was replaced by a ‘G’, ” said Yoshihiro Kawaoka, a virologist at the University of Wisconsin-Madison.

“Several articles had already described that this mutation makes the protein more functional and more efficient to enter cells,” Kawaoka said.

However, that earlier work relied on a pseudotyped virus that included the receptor-binding protein, but was not authentic, the researchers said.

Using reverse genetics, Baric’s team replicated a matching pair of mutant SARS-CoV-2 viruses encoding D or G at position 614 and compared basic property analysis using cell lines, primary human respiratory cells, and mouse and hamster cells. .

Researchers at the University of Wisconsin-Madison conducted airborne transmission and replication studies with both the original virus and the mutated version.

They found that the mutated virus not only replicates about 10 times faster, but is also much more infectious.

The hamsters were inoculated with one virus or another. The next day, eight uninfected hamsters were placed in cages alongside infected hamsters.

There was a divider between them so they couldn’t touch, but air could pass between the cages.

The researchers began looking for replication of the virus in the uninfected animals on the second day. Both viruses were passed between animals through airborne transmission, but the timing was different.

With the mutant virus, the researchers saw transmission in six out of eight hamsters within two days, and all hamsters by day four.

With the parent virus, they saw no transmission on day two, although all exposed animals were infected on day four.

“We saw that the mutant virus transmits better in the air than the original virus, which may explain why this virus dominated humans,” Kawaoka said.

The researchers also examined the pathology of the two coronavirus strains.

Once the hamsters were infected, they exhibited essentially the same viral load and symptoms.

This suggests that while the mutant virus is much better at infecting hosts, it does not cause significantly worse disease, they said.

However, the researchers caution that the pathology results may not be true in human studies. PTI SAR SAR

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