In the immunization of mice with Sindbis virus, a central nervous system infection elicits greater cross protection against lethal challenges with Venezuelan equine encephalitis (VEE) virus than do infections initiated by extraneural routes. Infective Sindbis virus administered intraperitoneally, subcutaneously or intravenously was considerably less cross protective than a single inoculation of the virus into the cerebrum, yet similar levels of homologous neutralizing antibody at 28 days post-inoculation were elicited by the host, regardless of the route by which the virus was administered. Cross protection was correlated with invasion by, and replication of, Sindbis virus within the central nervous system and histopathological changes in the brain. The lowest levels of VEE virus infectivity were recovered from the brains of mice previously infected with Sindbis virus by the intracerebral route.


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