The Gordon Wilson lecture: unique interactions between viruses, neurons and the immune system.
The increased susceptibility of young individuals to alphavirus encephalitis is likely to be linked to the ease with which immature neurons are induced to undergo apoptosis after infection. In the more mature individuals, virus infection of neurons may not lead to apoptosis and in the absence of an effective immune response persistent infection is established. The major mechanism by which alphavirus infection of neurons is controlled is by production and local secretion of antibody to the surface glycoproteins. Antibody acts synergistically with interferon to decrease intracellular virus replication but does not eliminate the infected cell or the viral RNA within the cell. Therefore, the immune response controls, but does not cure the infection, leading to a requirement for long-term local synthesis of antiviral antibody in the CNS. For the host persistent intracellular RNA and need for longterm control is probably a reasonable price to pay for a noncytolytic mechanism for control of neuronal viral infection.
Griffin
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Department of Molecular Microbiology and Immunology, Johns Hopkins University School of Public Health, Baltimore, Maryland 21205, USA.
D018354:Alphavirus Infections / Q000209:etiology / Q000276:immunology / Q000821:virology; D000818:Animals; D000914:Antibodies, Viral / Q000096:biosynthesis; D004671:Encephalitis, Arbovirus / Q000209:etiology* / Q000276:immunology / Q000821:virology; D006801:Humans; D051379:Mice; D008954:Models, Biological; D009474:Neurons / Q000821:virology; D012845:Sindbis Virus / Q000276:immunology / Q000472:pathogenicity / Q000502:physiology; D014779:Virus Replication / Q000276:immunology
D000914:Antibodies, Viral