Abstract

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has become a global public health menace because of its immunopathogenesis and faster transmission than prior coronaviruses that infected people. Due to the genetic similarity between SARS-CoV and MERS-CoV infections, knowledge from earlier SARS-CoV and MERS-CoV infections has been used to infer the mechanism behind the host immune response during the infection with SARS-CoV-2 even though this knowledge is incomplete. The hyperactivation of macrophages and monocytes, which results in autophagic cell death and increases interleukin-6 and neutrophil levels, is evidence for this. It has been proposed that SARS-CoV-2 undermines the host’s immune system by blocking interferon induction and signaling, which contributes to a cytokine storm that may result in acute respiratory distress syndrome and multiple organ failure while reducing the host’s adaptive immunological responses. This work gives a broad review of the molecular dynamics of SARS-CoV-2 infection from the viewpoints of molecular biology, virology, and immunology in order to clarify and critically characterize the immunopathogenesis of SARS-CoV-2 and how it can alter sickness severity. Thus, this would enlighten us on potential new therapeutic avenues for future studies.

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