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How Covid virus defeats body’s immune response

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New Delhi, Oct 22:  Japanese researchers have discovered that SARS-CoV-2, the virus responsible for Covid-19, carries an enzyme that can act against a cell’s innate defence mechanism against viruses.

This can answer why Covid-19 is more infectious than the previous SARS and MERS-causing viruses, said the researchers from Kobe University. The team focussed their study on the role of a molecular tag called “ISG15” in Covid virus that prevents nucleocapsid proteins from attaching to each other — a key process to enable viruses to assemble.

In addition, the “enzyme can remove the tags from its nucleocapsid, recovering its ability to assemble new viruses and thus overcoming the innate immune response,” explained virologist Shoji Ikuo from the varsity, in a paper in the Journal of Virology. While SARS and MERS viruses also carry an enzyme that can remove the ISG15 tag, Shoji’s team found that their versions are less efficient.

“The results suggest that the novel coronavirus is simply better at evading this aspect of the innate immune system’s defense mechanism, which explains why it is so infectious,” Shoji said.

The innate immune system is the first line of defense against pathogens which limits viral entry, replication, and assembly. It also detects and removes infected cells. Unlike SARS and MERS viruses, Covid rapidly spread to almost all continents, including the sparsely inhabited Antarctica.

The Covid virus continues to mutate and infect with newer variants. However, the severity has decreased with mass vaccinations and herd immunity. The new findings may pave the way to the development of more effective drugs against Covid-19 and possibly similar future diseases.

“We may be able to develop new antiviral drugs if we can inhibit the function of the viral enzyme that removes the ISG15 tag. Future therapeutic strategies may also include antiviral agents that directly target the nucleocapsid protein or a combination of these two approaches,” the researchers said.

IANS

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