In December 2019 an outbreak of the novel infectious virus SARS-CoV2 occurred and immense research is currently going on to contain the virus. Being a novel virus it is highly important to learn how the immune system has responded to the past viral infections in particular to the coronavirus family.

In December 2019 an outbreak of the novel infectious virus SARS-CoV2 occurred and immense research is currently going on to contain the virus. Being a novel virus it is highly important to learn how the immune system has responded to the past viral infections in particular to the coronavirus family.

A foreign invader (bacteria or virus) in a host system results in the activation of the immune response through a series of signaling events mediated by several proteins. Most Toll-like receptors (TLR), which bind bacterial or viral molecules and thereby detect the invasion, use the universal adaptor protein Myeloid differentiation primary response protein (MyD88) to initiate the immune response. TLRs activate NFkB, a key protein in the innate and adaptive immune response, through a signaling cascade, in which MyD88 plays an important role (Hoebe et al, 2003, Yamamoto et al, 2003). MyD88 induces phosphorylation of interleukin-1 receptor-associated kinase 1 (IRAK-1) resulting in NFkB activation and degradation of inhibitor kBalpha (IkBalpha). NFkB thereby translocates from cytosol to nucleoplasm and binds to the corresponding NFkB binding site in the promoter region of target genes resulting in expression of pro-inflammatory cytokines and adhesion molecules (Arancibia et al, 2007, Thompson et al, 2011).

The function of MyD88 in the protection against other types of coronavirus was studied earlier. Upon infection of mice with recombinant SARS-CoV, MyD88-/- mice resulted in increased weight loss, viral load and death as compared to wild type mice with only transient weight loss (Sheahan et al, 2008). A recent report suggests a therapeutic strategy against the SARS-CoV2 by inhibiting the upregulation of IL-1 beta, IL-6, TNF and CCL2 by suppressing MyD88 (Conti et al, 2020). MyD88 is crucial against several other viral infections including Vesicular stomatitis virus (VSV) (Lang et al, 2007), West Nile virus (WNV) (Szretter et al, 2010), Herpes simplex virus 1 (HSV-1 and HSV-2) (Mansur et al, 2005, Sørensen et al, 2008 ).

More studies will provide insights into the role of MyD88 in SARS-Cov2 infection in order to develop potential therapeutic approaches to control COVID-19 thereby improving health and socio-economic situation.

Jayasankar Kaimal