Coronavirus infection of the central nervous system: host-virus stand-off.
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.
Bergmann
Cornelia C
CC
Cleveland Clinic Foundation, Neurosciences, 9500 Euclid Avenue NC30, Cleveland, Ohio 44195, USA.
Lane
Thomas E
TE
Stohlman
Stephen A
SA
D000818:Animals; D002493:Central Nervous System Diseases / Q000276:immunology* / Q000821:virology*; D018352:Coronavirus Infections / Q000276:immunology* / Q000821:virology*; D007113:Immunity, Innate / Q000276:immunology; D051379:Mice; D006517:Murine hepatitis virus / Q000276:immunology / Q000472:pathogenicity / Q000502:physiology*; D013601:T-Lymphocytes / Q000276:immunology / Q000821:virology; D014779:Virus Replication