If viral infection persists for a long time, mutations accumulate and act as ‘evolutionary pressure’
Researchers at Tel Aviv University in Israel, thesis in ‘Nature Medicine’
A scanning electron microscope image of the novel coronavirus (red) emerging from the surface of cultured cells.
[미국 국립 알레르기 감염병 연구소(NIAID). 재판매 및 DB 금지]
(Seoul = Yonhap News) Reporter Ki-cheon Han = Recently, the number of confirmed cases of COVID-19 in European countries such as Germany, France and Italy is rapidly increasing once more.
Omicron sub-mutation BA with stronger propagation power. 4, BA·5 seem to spread quickly.
The novel coronavirus mutates faster than other existing viruses.
If this problem is not resolved, it is difficult to predict when the corona pandemic (pandemic) will end.
Finally, Israeli scientists have uncovered how the new coronavirus mutation, which does not respond well to neutralizing antibodies, occurs.
Chronic COVID-19 patients with weakened immunity were more likely to develop this type of corona mutation.
If the immune response weakens the antibody response in the lower airways of COVID-19 patients due to immune compromise, the virus can mutate several times during the longevity of the infection, scientists explained.
The results of this study conducted by Professor Addy Stern’s team at Tel Aviv University’s School of Biomedical Medicine were recently published as a paper in the journal Nature Medicine.
If there is no deletion in the gene sequence of the new corona 19, different types of antibodies (green and red) will stick to the new corona. (left)
Conversely, when a defect occurs, another antibody (red) binds to the novel coronavirus instead of a neutralizing antibody. (right)
If these gene sequence deletions in the novel coronavirus evolve, neutralization of antibodies can be avoided.
[미국 피츠버그대 Kevin McCarthy and Paul Duprex. 재판매 및
DB 금지]
According to the outline of the paper published on the American Association for the Advancement of Science (AAAS) site (www.eurekalert.org) on the 27th, the evolutionary pattern of the novel coronavirus following the outbreak of the corona pandemic puzzled scientists.
In the first year, the pace was generally slow with no major changes.
However, from the end of 2020, corona mutations with multiple mutations began to appear one following another.
Then, various hypotheses linking chronic COVID-19 patients with corona mutations were raised.
However, no studies have so far proven the association.
Professor Stern’s team noted that any population group will develop chronic COVID-19 patients.
So, an experimental group was composed of chronic COVID-19 patients from Soraski Medical Center in Tel Aviv.
These patients, without exception, had compromised immunity. Immune damage refers to a condition in which a part of the immune system malfunctions and does not function properly.
The risk of recurrent infections is also high if the novel coronavirus remains in the body of these patients for a long period of time without being eradicated.
In biological terms, these patients are like ‘incubators’ for creating viral mutations.
The new coronavirus stays in the body of patients with weakened immunity and accumulates mutations to adapt to the immune system.
This means that it mutates and avoids an attack on the immune system.
Human lung tissue generated in a mouse model by stem cell transplantation.
Novel coronavirus particles (green) infected with macrophages are clearly visible.
[미국 보스턴대 Douam and Kenney, 하버드의대 전자현미경 설비 협조. 재판매 및 DB 금지]
In fact, the experimental results are insufficient to reach clear conclusions.
The weakened immune system of immunocompromised patients is likely to act as an evolutionary pressure for viral mutations.
However, a direct relationship between the COVID-19 treatment and virus mutation, which can be an evolutionary pressure in a similar principle, has not been revealed.
In addition, some chronic COVID-19 patients showed symptoms of reinfection and recovered once more.
Oddly enough, this patient’s swab test was negative, but his lungs were severely infected.
The scientists assumed that the virus that made the mutation in the lungs returned to the upper respiratory tract to infect it.
In either case, what they have in common is the detection of a mutant form of the virus.
The appearance of a mutant virus suggests that it has not yet reached a stage of full recovery.
This was similar to the ‘modus operandi’ that occurs when HIV infection is not sufficiently treated.
“People with compromised immunity can become an incubator for the next mutated virus, regardless of their high risk of infection,” said Professor Stern.
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