Fig. 1.

Mechanism of inflammation during SARS-CoV-2 infection.

SARS-CoV-2 invade host cells with angiotensin-converting enzyme2 (ACE2) receptors present on the cell surface membrane. Virus nucleocapsid (N) protein hijack the host interferon type-1 signalling for the successful replication, transcription, and new viral progeny. Infected host cells undergo pyroptosis and release numerous proinflammatory cytokines (IL-6, IL-2, and TNFα) DAMPs and PAMPs. These free contents recognized by the neighboring cells and proceed with the same process of pyroptosis by using the NLRP3 receptor and also trigger the proinflammatory cytokines synthesis by TLR4-Nf-κB pathway. Monocytes (transform later into macrophage) and T-lymphocytes are attracted to the infected site and promote further pro-inflammation events, resulting in cytokine storm damage to the lung and other organs in the body.

TLR4: Toll like receptor 4; Myd88: Myeloid differentiation primary response 88; IL-1β: Interleukin 1 beta; IL-18: Interleukin 18; DAMPs: Death- associated molecular pattern; PAMPs: Pathogen-associated molecular pattern; NLRP3: Nucleotide-binding domain (NOD)-like receptor protein 3; ASC: Apoptosis-associated speck-like protein containing a CARD; IL-6: Interleukin 6; IL-2: Interleukin 2; TNFα: Tumor necrosis factor alpha; STAT: Signal transducer and activator of transcription; JAK: Janus kinase.