Pathogenicity and Persistence of Mouse Hepatitis Virus in Inbred Strains of Mice

  • Jean-Louis Virelizier
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 142)


Typical virus infections are short in incubation, acute in course, and rapid in their progress to either death or recovery. Some viruses, however, are able to escape host defense mechanisms and persist for long periods of time, often indefinitely. The pathogenesis and mechanisms of virus persistency vary widely according to the type of model considered. With scrapie, mink encephalopathy, kuru and Creutzfeld-Jacob disease, the infection elicits no inflammatory response. Apparently, immunological factors neither control nor complicate the disease. In other models, the virus persists in the face of an active host immune response. Two situations may be distinguished: the virus may be actively replicated by host cells, and viremia persists until the death of the host. This is true, for example, of lactic dehy-drogenase virus infection, Aleutian mink disease or equine infectious anemia. In these cases the virus circulates as infective immune complexes made of virus particles and specific antibody. Alternatively, like in herpes simplex and varicella-zoster infection, the virus remains latent and able to persist in cells of the nervous system. A permanent cell-mediated immune control is exerted on these infected cells, so that the virus is not actively replicated. Diminution of the effectiveness of T cell-mediated responses, for example during immunosuppressive therapy, allows reactivation of the infection.


Viral Antigen Choroid Plexus Mouse Hepatitis Virus Mumps Virus Equine Viral Arteritis 
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Copyright information

© Springer Science+Business Media New York 1981

Authors and Affiliations

  • Jean-Louis Virelizier
    • 1
  1. 1.Groupe d’Immunologie et de Rhumatologie Pédiatriques INSERM U 132Hopital des Enfants MaladesParisFrance

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