Virus disease as a consequence of viral pathogenicity and the anti-viral immune response.
The brief description of two virus systems, influenza and infectious bursal disease, shows enigmatically how at least two requirements must be met to render a virus pathogenic: the array of the whole genome rather than the formation of a particular "pathogenicity gene" and the capacity of the host cell to provide the appropriate microenvironment for an optimal posttranslational processing of structural proteins. In the case of influenza viruses this relates particularly to the cleavability of the haemagglutinin. Efficient virus replication in cells of vital importance, however, does not necessarily result in the development of pathological conditions, as in Borna disease, where neural cells are loaded with virus, and the disease is mediated by a T cell immune response. Immunological stimuli against this virus do not induce neutralizing antibodies which could mount a protective immunity. Infection with influenza viruses is inhibited by neutralizing antibodies, but the course of the disease in an infected organism is largely influenced by virus-specific antibodies which block virus release. It is difficult, however, to evaluate the effectiveness of this type of mechanism directed against the infected cell besides antibody-dependent and cell-mediated cytolysis.
Rott
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Institut für Virologie, Justus-Liebig-Universität Giessen, Germany.
Becht
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D000818:Animals; D006801:Humans; D007243:Infectious bursal disease virus / Q000276:immunology / Q000472:pathogenicity; D007251:Influenza, Human / Q000276:immunology / Q000382:microbiology; D009975:Orthomyxoviridae / Q000472:pathogenicity; D012088:Reoviridae Infections / Q000276:immunology / Q000382:microbiology; D014777:Virus Diseases / Q000276:immunology* / Q000382:microbiology*; D014780:Viruses / Q000276:immunology / Q000472:pathogenicity*