This project seeks to define determinants of acute CNS demyelination and disease recurrence 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 major features of HSV epidemiology and pathology are consistent with a hypothesis that HSV-2 is etiologic in MS. During FY 1985, studies published or in press have provided 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 suggests how HSV-2 could produce MS. Specifically, they show for the first time that: 1) When mice are infected by a natural genital route, some animals develop an acute, non-fatal CNS demyelinative disease, while others develop other clinically recognized neurological syndromes, including non-fatal meningitis and fatal panmyelitis. Other mice have no detectable CNS lesions. In man, similar mechanisms could produce non-fatal CNS demyelinative disease in genital HSV-2 infection. 2) Severe infections in mice are accompanied by an acute necrosis of thymic cortical lymphocytes, raising the possibility that severe disease may be due to a virus-induced supression of immunological function. Experiments in newborn mice show that virus can lytically infect some lymphoid tissues (spleen, lymph nodes) but not others (thymus). A direct virus effect on lymphoid tissues is a possible mechanism of immunosuppression.

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