Why is it difficult for Omicron to invade the lungs?

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Why is it difficult for Omicron to invade the lungs?

The team of Professor Ravindra Gupta, a virologist at the University of Cambridge in the United Kingdom, can provide a molecular explanation for Omicron’s lack of “power” in the lungs.

Omicron becomes “upper respiratory disease”?

In the past month, many research teams around the world have observed and studied Omicron variants.

They believe that despite the surge in Omicron infection cases, the hospital admission rate is not high, and compared with other variants, it causes fewer severe illnesses.

Recently, a report published by a global multinational research team also reached the same conclusion, that is, “Omicron is indeed milder than variants such as Delta.”

On December 29, scientists in Japan and the United States found that multiple studies on rodents showed that Omicron caused much less harmful infections, mainly confined to the upper respiratory tract: nose, throat, and respiratory tract; and damage to the lungs Much smaller.

The previous variants of the new coronavirus often cause lung damage and severe breathing difficulties. The study also found that animals infected with Omicron lost less weight and had lower mortality rates.

Omicron’s more gentleness may be an anatomical problem.

Dr. Michael Diamond, a virologist at the University of Washington, and his colleagues found that the level of Omicron virus in the nose of hamsters is the same as that of animals infected with the early new coronavirus, but the level of Omicron virus in their lungs is only one-tenth of that of other variants, or even more.

In addition, researchers from the University of Hong Kong have similar findings.

They studied some tissues removed from the human respiratory tract during the operation and found that Omicron grew slower in 12 lung samples than Delta and other variants.

Researchers also studied infections of bronchial tissues, the tubes that transport air to the lungs, and found that Omicron grew faster in these bronchial cells than Delta or the original new coronavirus.

This may explain why Omicron has a higher concentration level in the upper respiratory tract.

Scientists also said that these findings need further research.

For example, testing on monkeys, or examining human respiratory tracts that are actually infected with Omicron;

once further corroboration is obtained, it can explain why the admission rate of Omicron infection is lower than that of Delta and other variants.

Why is it difficult for Omicron to invade the lungs?

The team of Professor Ravindra Gupta, a virologist at the University of Cambridge in the United Kingdom, can provide a molecular explanation for Omicron’s lack of “power” in the lungs.

Data show that many cells in the lung carry a protein called TMPRSS2 on the surface, and this protein helps the virus to enter the lung cells.

Dr. Gupta’s team discovered that Omicron could not grasp the TMPRSS2 protein firmly. Therefore, Omicron’s ability to infect lung cells in this way is worse than Delta.

A research team from the University of Glasgow in the UK also independently came to the same conclusion.

At the same time, the virus can also infect cells that do not make TMPRSS2 protein through another way, because cells located at higher positions in the respiratory tract often do not carry this protein, which may also explain why the level of Omicron in the upper respiratory tract is higher. .

Dr. Gupta speculates that Omicron has become an “upper respiratory disease”, mainly destroying the throat and nose.

This also means that the variant is more likely to be discharged into the air in the form of droplets and easily encounter its new host.

So scientists already know that Omicron is highly contagious partly due to its ability to evade antibodies, so it can infect vaccinated people more easily than other variants.

However, Omicron may also have other biological advantages. Last week, researchers reported that a variation of this variant may weaken the body’s innate immunity.

It is an alarm system that quickly activates the human immune system when the virus enters the nose and the first sign of invasion appears. But this also needs more experimental verification.