SARS-CoV-2 Induced Innate Immune Responses Vary with Disease Severity

A team of researchers from China and Germany has conducted a large meta-analysis using transcriptome data of SARS-Cov-2 t evaluate the routes of viral entry and the characteristics of innate immune responses induced by SARS-CoV-2 infection. The scientists analyzed a diverse set of publicly available transcriptome data of SARS-CoV-2, SARS-CoV, and MERS-CoV. These data have been obtained from different types of cells. The scientists have observed that higher expression levels of host cell receptors, such as ACE2 or DPP4, do not influence the infection efficiency of SARS-CoV-2 or MERS-CoV. Moreover, the infection efficiency of human coronaviruses has been found to vary with cell types and viral load. The SARS-CoV-2 can enter human cells that do not express TMPRRS2 or TMPRSS4, which are cellular proteases essential for the priming of the viral spike protein.

However, they have observed that for TMPRRS2 or TMPRSS4 independent entry of SARS-CoV-2, the host cells need to express cathepsin B and cathepsin L, which are endosomal proteases required for viral entry through the endocytic pathway. These observations suggest that receptor-mediated endocytosis could be an alternative route of SARS-CoV-2 entry. Expressions of interferon, pro-inflammatory mediators, and interferon-stimulated genes in various cell types as well as in biological samples obtained from COVID-19 patients were analyzed to determine the strength of innate immune responses. The findings reveal that moderately and severely affected COVID-19 patients display significantly increased expressions of interferons, interferon-stimulated genes, and pro-inflammatory cytokines. In contrast, samples with an inadequate viral infection have shown low levels of interferons and moderate induction of interferon-stimulated genes.

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