Medical scientists have found out that the cell types, which the SARS-CoV-2 — the virus cause Covid-19 — infects, makes it even more deadly.
The research, led by Jose Ordovas, doctoral student at Boston Children’s Hospital, in the US, has found that one of the body’s primary defence against viral infections might help the Covid to infect those primary defensive cells which protects us from infections.
The findings, that are published by the journal Cell, will helps in focusing the efforts to understand what SARS-COV-2 does to our body, why some people are more immune against it, and how best to search for treatments, the researchers say.
Recent research displayed the results which tells that SARS-CoV-2 uses a acceptor called ACE2 to gain entry into human cells, assisted by an enzyme called TMPRSS2.
In the study, the team studied single-cell RNA sequencing, which results which out of roughly 20,000 genes are “on” in single cells. They found out that only a small percentage of human respiratory and intestinal cells, often very much lower than 10 per cent, for both ACE2 and TMPRSS2.
Further, the research showed that the ACE2 gene, which encodes the receptor which is used by SARS-CoV-2 to enter human cells, is revived by interferon — one of the body’s primary defence when it detects a virus. Interferon converted the ACE2 gene to even higher levels, possibly giving the virus new ways to get in.
Interferons, in fact, are being used and tested as a treatment for Covid-19. Would they be of help, or would they do more harm than good? That’s not clear yet.
It might be possible that in some cases, because of the timing of the dose, interferon can suppress the virus, while in some, interferon promotes more infection.
The new findings might also raise some new paths of inquiry around ACE inhibitors. These drugs are most commonly used to cure hypertension, which has been connected to more severe Covid-19 disease.(IANS)

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