Coronavirus infection of the central nervous system: host-virus stand-off

Nat Rev Microbiol. 2006 Feb;4(2):121-32. doi: 10.1038/nrmicro1343.

Abstract

Several viruses infect the mammalian central nervous system (CNS), some with devastating consequences, others resulting in chronic or persistent infections associated with little or no overt pathology. Coronavirus infection of the murine CNS illustrates the contributions of both the innate immune response and specific host effector mechanisms that control virus replication in distinct CNS cell types. Despite T-cell-mediated control of acute virus infection, host regulatory mechanisms, probably designed to protect CNS integrity, contribute to the failure to eliminate virus. Distinct from cytolytic effector mechanisms expressed during acute infection, non-lytic humoral immunity prevails in suppressing infectious virus during persistence.

Publication types

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

MeSH terms

  • Animals
  • Central Nervous System Diseases / immunology*
  • Central Nervous System Diseases / virology*
  • Coronavirus Infections / immunology*
  • Coronavirus Infections / virology*
  • Immunity, Innate / immunology
  • Mice
  • Murine hepatitis virus / immunology
  • Murine hepatitis virus / pathogenicity
  • Murine hepatitis virus / physiology*
  • T-Lymphocytes / immunology
  • T-Lymphocytes / virology
  • Virus Replication