Middle East respiratory syndrome and severe acute respiratory syndrome

Curr Opin Virol. 2016 Feb:16:70-76. doi: 10.1016/j.coviro.2016.01.011. Epub 2016 Feb 12.

Abstract

The recent emergence of the Middle East respiratory syndrome (MERS)-CoV, a close relative of the Severe Acute respiratory syndrome (SARS)-CoV, both of which caused a lethal respiratory infection in humans, reinforces the need for further understanding of coronavirus pathogenesis and the host immune response. These viruses have evolved diverse strategies to evade and block host immune responses, facilitating infection and transmission. Pathogenesis following infection with these viruses is characterized by a marked delay in the induction of Type I interferon (IFN I) and, subsequently, by a poor adaptive immune response. Therapies that expedite IFN I induction as well as interventions that antagonize immunoevasive virus proteins are thus promising candidates for immune modulation.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Coronavirus Infections / immunology*
  • Coronavirus Infections / metabolism
  • Coronavirus Infections / transmission
  • Coronavirus Infections / virology*
  • Disease Susceptibility
  • Epitopes / immunology
  • Host-Pathogen Interactions / immunology
  • Humans
  • Immunomodulation
  • Middle East Respiratory Syndrome Coronavirus / physiology*
  • Severe Acute Respiratory Syndrome / immunology*
  • Severe Acute Respiratory Syndrome / metabolism
  • Severe Acute Respiratory Syndrome / virology*
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism

Substances

  • Epitopes