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This is why Omicron spreads 70 times faster and better than Delta

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New paper shows that the new variant of the coronavirus known as Omicron multiplies 70 times faster in the tissues that line the airways than the other variants

Researchers discovered that Omicron SARS-CoV-2 infects and multiplies 70 times quicker in human bronchi than the Delta variant and original SARS-CoV-2, which could explain why Omicron spreads faster between humans than earlier strains. Their research also revealed that the Omicron infection in the lungs is substantially lower than the initial SARS-CoV-2, which could indicate that the disease is less severe. This study is now undergoing peer review in preparation for publication.

The reason that the variant is SARS-CoV-2 Omicron spreading faster around the world is that it multiplies 70 times faster in the tissues that line the airways than the other variants of the coronavirus.

Omicron grows 70 times faster in tissues that lining airway passages than the older Delta variant, which may facilitate person-to-person dissemination, according to the researchers. However, Omicron replicates 10 times slower in lung tissues than the original coronavirus, which may lead to less severe sickness.

The research team has not published a formal report on the findings because it is being peer-reviewed for publication. Dr. Michael Chan Chi-wai, study leader, stated in a news release issued by Hong Kong University: “It is important to note that the severity of disease in humans is not determined only by virus replication” but also by each person’s immune response to the infection, which can sometimes evolve into life-threatening inflammation.

Chan further added, “By infecting many more people, a very infectious virus may cause more severe disease and death even though the virus itself may be less pathogenic. Therefore, taken together with our recent studies showing that the Omicron variant can partially escape immunity from vaccines and past infection, the overall threat from Omicron variant is likely to be very significant.”

According to the researchers, a structural model of how the Omicron type connects to cells and antibodies gives light on its behavior and will aid in the design of neutralizing antibodies.

With the help of computer modeling of the spike protein on Omicron’s surface, they assessed molecular interactions occurring when the spike attaches onto a cell-surface protein called ACE2, the virus’s gateway into the cell.

While the original virus shared a metaphorical handshake with ACE2, Omicron’s grip “look more like a couple holding hands with their fingers entwined,” according to Joseph Lubin of Rutgers University in New Jersey. Lubin stated that the “molecular anatomy” of the grip may help explain how Omicron’s mutations interact to aid in cell infection.

Additionally, the research team modeled the spike with various classes of antibodies attempting to target it. The antibodies strike from several angles, “like a football team’s defense might tackle a ball carrier,” Lubin explained, with one person grasping from behind and another from the front. Certain antibodies “appear likely to get shaken off,” while others appear to retain their effectiveness. Booster vaccines increase antibody levels, resulting in “more defenders,” which may partially compensate for an individual antibody’s “weaker grip,” Lubin explained.

The findings, which were published on Monday on the website bioRxiv in advance of peer review, require confirmation, “particularly with real-world samples from people,” Lubin added.

“While our molecular structure predictions are by no means a final word on Omicron, (we hope) they enable a faster and more effective response from the global community.”

Source: HKUMED

Image Credit: Reuters

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