A common mutation in the new coronovirus that allowed it to spread rapidly around the world could make it more susceptible to a vaccine, according to a study that proved some of the first concrete findings about SARS-CoV-2. , Which causes COVID-19, is growing.
Researchers at the University of North Carolina at Chapel Hill and the University of Wisconsin-Madison in the United States noted that a new strain of coronovirus, called D614G, has emerged in Europe and has become the most prevalent in world.
Their study, published in the journal Science, shows that the D614G strain is faster and more infectious than the virus, which originated in China, which spread at the start of the epidemic.
The D614G strain spreads quickly, but has not been associated with more severe disease in animal studies, and the strain’s antibody is slightly more sensitive to neutralization by drugs, the researchers said.
“The D614G virus increases parental stress approximately 10-fold and replicates extremely efficiently in primary nasal epithelial cells, a potentially important site for person-to-person transmission,” said Ralph Barrick. Chapel Hill, professor at UNC-.
Researchers believe that the coronovirus strain D614G is dominant because it enhances the ability of spike proteins to open cells to enter the virus.
The researchers said the D614G mutation caused the shutter to open after a peak, allowing viruses to infect cells more efficiently, but also to create a pathway for the weak nucleus of the virus, the researchers. said.
With an open shutter, it is easy for antibodies – such as the vaccines currently being tested – to infiltrate and inactivate the virus, he said.
“The original spike protein had a ‘D’ in this position, and it was replaced with ‘G’,” said Yoshihiro Kawaoka, a virologist at the University of Wisconsin-Madison.
Yoshihiro Kawaoka said: “Several articles have already reported that this mutation makes the protein in cells more functional and efficient.”
Previous work, however, relied on a pseudotyped virus that contained receptor binding proteins, but was not authentic, the researchers said.
Using reverse genetics, Ralph Baric’s team replicated a pair of mutant SARS-CoV-2 viruses encoding D or G at position 614 and used cell lines, primary human respiratory cells, and cells from mice and hamster. Benchmarking core assets using.
Researchers at the University of Wisconsin – Madison conducted airborne replication and transmission studies with the original virus and the mutated version.
They found that the mutated virus not only replicated about 10 times faster, but was much more infectious.
The hamsters were vaccinated with either virus. The next day, eight unaffected hamsters were placed in cages next to infected hamsters.
There was a separator between them so they couldn’t touch each other, but air could pass through the cages.
Researchers began looking for virus replication in animals without two animals on day one. Both viruses underwent airborne transmissions between animals, but the timing was different.
With the mutant virus, researchers observed six out of eight hamsters within two days and four days of transmission to all hamsters.
With the original virus, they saw no transmission on the second day, although all exposed animals were infected by the fourth day.
“We noticed that the mutant virus transmits better in the air than the original virus, which may explain why this virus is dominant in humans,” said Yoshihiro Kawaoka.
The researchers also studied the pathology of two strains of coronavirus.
Once infected, the hamsters showed essentially the same viral load and symptoms.
This suggests that while the mutant virus is much better at infecting hosts, it doesn’t cause significantly worse disease, he said.
However, the researchers warn that the results of the pathology in human studies may not be precise.
(Except for the title, this story was not edited by NDTV staff and posted from a syndicated feed.)