Why does the omicron strain not cause severe disease?

Recent research shows that the micronized strain grows in the airways and multiplies more slowly in the lungs.

The researchers said that major differences between the emicron and other strains of the coronavirus could help predict the effects of the emicron, the researchers said.

“Compared to the delta strain, this strain multiplies 70 times faster in the tissues that cover the airways and may facilitate person-to-person spread, but the omicron strain multiplies 10 times slower in the lung tissue than the original version of the coronavirus,” they said. Probably leads to a milder illness.

It is noteworthy that the official report of the findings is under review for publication and has not yet been published by the research team.

“It is important to note that the severity of the disease in humans is not only determined by the replication of the virus, but also by the immune response of each individual to the infection, which sometimes leads to inflammation,” said Dr. Michael Chan Chi-wai, a researcher in the study. It becomes life threatening.

Chan added that a highly contagious virus can cause more severe illness and death by infecting more people, even if the virus itself is less pathogenic. Therefore, the results of our recent research show that the omicron strain escapes some of the immunity from vaccines and natural immunity, so the overall threat of the omicron strain is probably very important.

According to the researchers, a structural model of how the omicron strain binds to cells and antibodies could determine its behavior and help design neutralizing antibodies.

Using computer models of omicron-level spike proteins, the researchers analyzed the molecular interactions of the spike on a cell surface protein called ACE2, the gateway for the virus to enter the cell.

“Metaphorically, the connection of the main virus to ACE2 is like a handshake, but the connection of the omicron to it is similar to when two people tie their hands together and squeeze,” said Joseph Lubin of Rutgers University in New Jersey.

“The molecular anatomy of an omicron may explain how omicron mutations work together to help infect cells,” Lubin said.

The team also modeled the spike with different classes of antibodies it tried to attack.

“Antibodies attack from different angles, and in this attack some antibodies are likely to be destroyed while others remain effective,” Lubin said.

“Boosting vaccines increase antibody levels and, as a result, create ‘more defenders’ that may partially compensate for the weakness of the antibody in some people,” he said.

“These findings have been published on the bioRxiv website and must be confirmed by actual samples of individuals before being examined by their counterparts,” he said. Although our predictions of molecular structure are by no means the final result of the micron, we hope to generate a faster and more effective response from the international community.

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