This project seeks to define the spectrum of acute and recurrent CNS and peripheral disease, including CNS demyelination, which is produced in experimental herpes simplex virus type 2 (HSV-2) infection, and to refine and test a hypothesis which relates HSV-2 infection to the human demyelinative disease, multiple sclerosis (MS). Our previous studies suggest that several major features of HSV epidemiology and pathology are consistent with the hypothesis that HSV-2 is etiologic in MS. During FY 1986, studies published or submitted provide evidence which further defines the spectrum of experimental disease produced by HSV-2 in the CNS and in lymphoid tissues. These studies provide insights into human infections and disease which HSV-2 is known to cause, and suggest how HSV-2 could produce a CNS demyelinative disease. Specifically, they show that: 1) When mice with latent HSV-2 infections, previously established by a genital route, are immunosuppressed, virus can again be isolated from the genital tract. In this reactivation model, virus can be demonstrated by virus isolation or antigen detection methods in the spinal cord, brain and spleen tissues. Virus is also found in 2 distinct groups of dorsal root ganglia, where viral antigen is present in neurons, endoneurial cells, and axons. In this model, viral latency, reactivation, nervous system disease can be studied, and vaccine efficacy can be tested. 2) At early stages of primary infection, virus is first detected in sensory roots, then spreads to the spinal cord. This study provides further evidence that HSV-2 spreads to the CNS chiefly via peripheral nerve roots, probably in the intra-axonal compartment.

National Institute of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
Intramural Research (Z01)
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