Molecular Insights into Severe Acute Respiratory Syndrome Coronavirus 2 Pathobiology: Dissecting the Interplay between Cellular Innate Immunity and Immune Evasion

Crit Rev Immunol. 2020;40(6):485-496. doi: 10.1615/CritRevImmunol.2020035855.

Abstract

In December 2019, outbreak of a novel coronavirus flared in Wuhan, the capital city of Hubei province, China. The identified pathogen was an enveloped RNA betacoronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The outbreak was declared a pandemic by the World Health Organization (WHO), because the continual spread of this deadly and highly infectious virus is a health emergency for all world nations. SARS-CoV-2 is associated with severe atypical pneumonia coronavirus disease-19. Typical symptoms of this disease include fever, malaise, cough, shortness of breath, and in severe cases, death. As the virus continues to invade host cells deep into alveoli, infection severity mostly depends on the undeterred immune response that is triggered by elevated levels of inflammation-inducing cytokines, called a cytokine storm. In this article, we provide a comprehensive review of the viral life cycle and immunological responses associated with the SARS-CoV-2 infection.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • COVID-19 / diagnosis
  • COVID-19 / epidemiology
  • COVID-19 / etiology*
  • COVID-19 / therapy
  • Cytokine Release Syndrome / diagnosis
  • Cytokine Release Syndrome / etiology
  • Cytokine Release Syndrome / therapy
  • Disease Susceptibility* / immunology
  • Host-Pathogen Interactions / immunology*
  • Humans
  • Immune Evasion
  • Immunity, Cellular
  • Immunity, Innate
  • SARS-CoV-2 / physiology*
  • Severity of Illness Index