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Researchers set to determine hallmarks of Covid-19 severity

Prashasti Awasthi Mumbai | Updated on February 17, 2021

A new study investigated the hallmarks of Covid-19 severity to determine the primary influencer of the major illness.

The findings of the study were published in the journal Nature. For the study, the authors analysed cells, including immune cells, in blood samples from 21 people with Covid-19 and 25 uninfected individuals who were either healthy or had a lung injury or breathing difficulties.

They monitored gene expression during the course of the infection as patients went on to develop either what was categorised as mild–moderate or severe Covid-19.

The authors found that the cells of people with mild–moderate Covid-19 expressed a distinct set of genes. This expression depends on what are known as type I interferon proteins. Interferons, molecules that are also called cytokines, drive the expression of genes that have a role in antiviral defense.

This interferon-regulated gene-expression signature was not observed in the cells of people with severe Covid-19.

Notably, the researchers found a similar program is associated with another form of severe disease called sepsis in patients with Covid-19 severity. Sepsis occurs due to an aberrant immune response to bacterial infection.

The researchers speculated that the lack of activation of this program in people with severe Covid-19 could contribute to the observed differences in disease severity.

Reason behind lack of interferon-regulated gene-expression

The authors found that the level of antibodies against the SARS-CoV-2 spike and nucleocapsid proteins was higher in people with severe disease than in those with mild–moderate Covid-19.

Moreover, high antibody levels were negatively correlated with the presence of cells expressing an interferon-regulated gene-expression program, the study stated.

After further research, the authors found that the presence of plasma from people with severe disease blocked the induction of interferon-responsive genes. However, if this plasma was treated to deplete it of antibodies, interferon-mediated gene expression was restored in these immune cells.

In what the authors classified as mild–moderate cases of this illness, patients made antibodies that recognize the spike protein of the SARS-CoV-2 virus.

The authors reported that immune cells called monocytes and from these individuals express genes that are regulated by the protein interferon. However, a receptor called CD32B, which is found on monocytes, can dampen such immune responses if it is bound by another protein.

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Published on February 17, 2021
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