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The lethal encephalitis caused in mice by Semliki Forest virus (SFV) is modulated to a subclinical infection by administration of defective interfering SFV, although virus still multiplies both in the central nervous system (CNS) and systemically. Here we report that such infections result in unique and selective changes in the normal levels of CNS neurotransmitters some of which persist after infectious virus can no longer be detected. This represents a previously undocumented category of infection which may have a bearing on the aetiology of those human neurological and neuropsychiatric diseases to which viruses are believed to contribute.
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