SARS-CoV-2 mediated dysregulation in cell signaling events drives the severity of COVID-19

A balance in immune response against an unfamiliar pathogen is crucial to eliminate the infection. A cascade of cell signaling events is immediately activated upon sensing the presence of SARS-CoV-2 by cellular toll like receptors in a natural host response manner against the invading virus. The ultimate aim of such innate immune signaling pathways is to provide a required level of protection to our bodies by interfering with the invader. However, if there is any loss in such balance, an impairment in immune system emerge that fails to control the regulated transcription and translation of signaling components. Consequently, excessive level of proinflammatory mediators release into the circulatory systems that ultimately cause “cytokine storm” and COVID-19 pathological syndromes. The limited production of interferons (IFNs), while excessive yield of pro-inflammatory cytokines followed by SARS-CoV-2 infection suggests an abnormal cell signaling event and explains the reasons of increased immunopathology and severity in COVID-19.