SARS-CoV-2 infection mediates immune response, both innate and adaptive. The enhanced level of the innate response and decreased level of adaptive causes tissue damage. Upon viral infection, there is an immune response. T cells, especially the cluster of differentiation 4 (CD4+) and a group of differentiation 8 (CD8+), have an anti-viral role. CD8+ T cells are highly cytotoxic, and they killed infected cells. This T cell induces the pro-inflammatory cytokines through nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling. This process further activates the cytokines and chemokines [7]. Similar to SARS-CoV, MERS, SARS-CoV-2 infection in the immune effector cells are also having the enhanced level of the cytokines such as IFN-γ, IFN-α, IL-6, IL-1β, IL-18, IL-12, TGFβ, IL-33 and TNF-α and chemokines such as CCL2, CCL5, CCL3, CXCL10, CXCL9, and CXCL8. Similar to this, severe MERS-CoV infected patient's serum shows an increased level of the cytokines and chemokines. This cytokine storm further causes multiple organ failures to further leads to the death of the SARS-CoV-2 patient [109].