Individual genetic variability mainly of Proinflammatory cytokines, cytokine receptors, and toll‐like receptors dictates pathophysiology of COVID‐19 disease.

Innate and acquired immunity responses are crucial for viral infection elimination. However, genetic variations in coding genes may exacerbate the inflammation or initiate devastating cytokine storms which poses severe respiratory conditions in coronavirus disease‐19 (COVID‐19). Host genetic variations in particular those related to the immune responses determine the patients' susceptibility and COVID‐19 severity and pathophysiology. Gene polymorphisms such as single nucleotide polymorphisms (SNPs) of interferons, TNF, IL1, IL4, IL6, IL7, IL10, and IL17 predispose patients to the severe form of COVID‐19 or severe acute respiratory syndrome coronavirus‐2 (SARS‐COV‐2). These variations mainly alter the gene expression and cause a severe response by B cells, T cells, monocytes, neutrophils, and natural killer cells participating in a cytokine storm. Moreover, cytokines and chemokines SNPs are associated with the severity of COVID‐19 and clinical outcomes depending on the corresponding effect. Additionally, genetic variations in genes encoding toll‐like receptors (TLRs) mainly TLR3, TLR7, and TLR9 have been related to the COVID‐19 severe respiratory symptoms. The specific relation of these mutations with the novel variants of concern (VOCs) infection remains to be elucidated. Genetic variations mainly within genes encoding proinflammatory cytokines, cytokine receptors, and TLRs predispose patients to COVID‐19 disease severity. Understanding host immune gene variations associated with the SARS‐COV‐2 infection opens insights to control the pathophysiology of emerging viral infections. [ABSTRACT FROM AUTHOR]