Studies show that Omicron is more like an upper respiratory virus
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Studies show that Omicron is more like an upper respiratory virus
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The most comprehensive in vitro virulence studies show that Omicron is more like an upper respiratory virus.
In recent days, studies on the virulence of Omicron have been released one after another, giving us more confidence in the “coexistence with the virus” life in 2022.
On January 2, 2022, Peacock, a scientist at Imperial College in the United Kingdom , published a very important preprint of Omicron’s virological characteristics submitted by him on Twitter, which is currently the most comprehensive study on Omicron’s in vitro virulence .
The title of these research papers is “the sars-cov-2 variant, omicron, shows rapid replication in human primary nasal epithelial cultures and efficiently uses the endosomal route of entry”.
This study is consistent with the conclusions of many previous studies that Omicron has low lung toxicity ; it is more like an upper respiratory virus, especially the susceptible nasal mucosa .
Studies have found that in primary human nasal mucosal epithelial cells (hNECs), Omicron is more likely to infect hNECs than other mutants, and has a stronger ability to replicate in hNECs.
The more important finding is that in addition to being susceptible to human ACE2 receptor cells, Omicron is also susceptible to murine ACE2 receptor cells, and it is also susceptible to birds and chrysanthemum bat cells.
This characteristic is not seen in other mutant strains. Therefore, the author predicts Omicron It can be reverted to animals, causing virus epidemics in animals .
Another feature of Omicron has also been proven by previous studies, that is, it does not cause cell-cell fusion (fusogenic) like other mutant strains, which may also be a reason for its reduced virulence.
In addition, Omicron’s two mutations N679K and P681H at the Furin cleavage site can enhance S1/2 cleavage, and therefore can increase its infectivity .
However, Omicron does not use TMPRSS2 to enter cells like other mutant strains, so TMPRSS inhibitors cannot effectively inhibit Omicron from entering cells; on the contrary, TMPRSS inhibitors can inhibit Delta mutant strains from entering cells.
Omicron enters the cell more easily through the endosome. Because it does not rely on TMPRSS, Omicron has low selectivity for cell entry, which allows it to infect more types of cells, but it may be a reason for its low pneumophilicity .
This research is very serious and meticulous. It is a classic research in virology and I believe it will soon be accepted by top journals such as Cell.
references:
https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/1043652/S1454_Omicron_report_20.12_Imperial.pdf
Studies show that Omicron is more like an upper respiratory virus
(source:internet, reference only)
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