Common coronavirus mutations actually make COVID-19 more susceptible to vaccination.


Defeating COVID-19 coronavirus

Mutations are not expected to interfere with the effectiveness of the vaccine under development.

A new study was published in Science Confirms it SARS-CoV-2 Has mutated in a way that has enabled it to spread rapidly around the world, but the spike mutation could make the virus more susceptible to vaccination.

A new strain of coronavirus, called D614G, has emerged in Europe and has become the most common in the world. Research from the University of North Carolina at Chapel Hill and the University of Wisconsin-Madison has shown that the D614G strain replicates faster and is more transmissible than the virus that originates in China, which spreads early in the epidemic.

The study findings had bright spots: while the D614G strain spread rapidly, in animal studies it was not associated with more serious disease, and the strain is slightly more susceptible to neutralization by antibody drugs.

The study, published on November 12, 2020, provides some of the first concrete findings about how SARS-COV-2 is evolving.

U.N.C. “The D614G virus advances ancestral strains by about 10 times and replicates very effectively in primary nasal epithelial cells, which is a potentially important site for person-to-person transmission,” said Ralph Barrick, professor of epidemiology at NA. Said Ralph Barrick, professor of epidemiology at UNC. -Professor of Microbiology and Immunology at Chapel Hill Gillings School Global Public Health and UNC School Medicine Medicine.

Barrick has studied coronavirus for more than three decades and was instrumental in the development of remedesivir, the first FDA-approved treatment COVID-19.

The researchers believe that the D614G strain of the coronavirus is dominant because it increases the ability of spike proteins to open cells to enter the virus. These crown-like spikes give the coronavirus its name.

The D614G mutation causes a spike at the top of a spike that pops open, allowing the virus to infect cells more effectively, but also paving the way for a virus-sensitive core.

With a flop open, it’s easy for antibodies – like the vaccines currently being tested – to infiltrate and inactivate the virus.

For a recent study, Berry Lab researchers – including the first author Yuxuan J. Howe included – both virologists from the University of Wisconsin-Madison faculty, Yoshiho Kawaoka and Peter Hoffman.

The original spike protein had a ‘D’ on this condition and was replaced by a ‘G’, Kawoka said. “Some papers have already described that this mutation makes proteins more functional and more efficient for entering cells.”

Previous work, however, relied on pseudotype viruses that contained receptor-binding proteins but were not authorized. Using contrast genetics, Barrick’s team created a matched pair of mutant SARS-CoV-2 viruses that encoded at D or G status 614 and compared the original property analysis using cell lines, primary human respiratory cells, and mouse and hamster cells.

Kawaoka and Huffman have contributed to the model Dell of their unique coronavirus study, which uses hamsters. A University of Wisconsin-Madison team – including Shiho Chiba, who conducted hamster experiments – studied replication and airborne transmission with both the original virus and the modified version created by Barrick and Howe.

They found that mutated viruses replicate only 10 times faster – they are even more contagious.

Hamsters were inoculated with one virus or another. The next day, eight uninfected hamsters were placed in a cage next to the infected hamster. There was a divider between them so they could not touch, but air could pass between the cages.

The researchers began searching for the virus in non-protected animals the next day. Both viruses underwent airborne transmission between animals, but the time was different.

With the mutant virus, the researchers observed migration from eight hamsters in six days to two days and in all four days to all hamsters. From the original virus, they did not see any transmission the next day, however, all exposed animals were infected for four days.

“We found that mutant viruses transmit better airborne fluids than that [original] The virus, which could explain why it is so prevalent in humans, “said Kawoka.

The researchers also examined the pathology of two coronavirus strains. Once the hamsters became infected, they presented similar viral loads and symptoms. (Mutants with mutated strains lose slightly more weight during illness.) This suggests that mutant virus is better in infected hosts, not significantly worse.

Researchers have warned that the results of the pathology may not be true in human studies.

“SARS-Cavi-2 is a completely new human pathogen and its evolution in the human population is difficult to predict,” Barrick said. “Similar to the recently discovered Mink SARS-Covy-2 Cluster 5 variant in Denmark, new variants are constantly emerging that encode the D614G.

“To protect public health as much as possible, we must continue to track and understand the consequences of this new change on disease severity, transmission, host range and vulnerability to vaccine-induced immunity.”

Reference: “SARS-CO-2D614G variant, efficient replica in vivo showing ex vivo and transmission” Yixuan J. Howe, Shiho Chiba, Peter Hoffman, Camille Ehre, Makoto Kuroda, Kenneth H. Dinnon III, Sarah R. List, Alexandra Schaefer, Noriko Nakajima, Kenta Takahashi, Rihanna E. Lee, Teresa M. Massenic, Rachel Graham, Caitlin E. Edwards, Longping v. Tse, Kenichi Okuda, Elena J. Markman, Luther Bartlett, Arvinda de Silva, David M. Margolis, Richard c. Boucher, Scott H. Randall, Tadaki Suzuki, Lisa E. Gralinski, Yoshihiro Kawaoka and Ralph S. Barrick, 12 November 2020, Science.
DOI: 10.1126 / Science.Be 8499