Neurogenic spread of Semliki Forest virus in mice.
We present evidence that in SFV-infected mice the virus invades the brain via nervous tracts, and that in the early stage of infection of the brain itself dissemination is restricted to neurons. After intranasal (i.n.) application, migration along the neuronal route appeared to be the principle mechanism of spread irrespective of the virulence of the strain used. After subcutaneous (s.c.) infection, neuronal spread could also be demonstrated, however the pattern and time course of brain invasion were different. The LD50 of strain Hd depended significantly on the route of virus application: compared with the i.n. route, its value increased after s.c. infection. This increase was correlated with high plasma interferon induction and natural killer cell activation. In contrast, these activities were virtually absent during the early course after i.n. infection.
D000281:Administration, Intranasal; D000818:Animals; D004660:Encephalitis / Q000276:immunology / Q000382:microbiology*; D007111:Immunity, Cellular; D007372:Interferons / Q000096:biosynthesis; D007694:Killer Cells, Natural / Q000276:immunology; D051379:Mice; D012672:Semliki forest virus / Q000254:growth & development*; D014018:Tissue Distribution; D014036:Togaviridae Infections / Q000276:immunology / Q000382:microbiology*
D007372:Interferons