Several studies ( 1,2,3) have suggested that lethality in acute lymphocytic choriomeningitis (LCM) virus infection of mice is a result of host immunologic response, rather than a direct effect of virus multiplication. Mice inoculated neonatally are protected from lethal effects of the virus, while adult morbidity and mortality can be reduced or delayed by various immunosuppressive methods, including X-irradiation, antimetabolite therapy, and neonatal thymectomy ( 1,2). In the present study, the role of cellular immunity in LCM palthogenesis was further examined, using rablbi t anti-mouse thymo-cyte (RAMT) serum to inhibit host response.Materials and methods. Three-to fourweek-old ICR mice of both sexes were used in all experiments. RAMT serum was prepared as described previously (4), by immunizing rabbits over a several-week period with dispersed suspensions of viable mouse thymus cells. Serum effectiveness was assayed by its ability to (a) diminish peripheral blood lymphocyte counts by 50% within a 4-hour period, and to (b) double the mean survival time of AKR skin grafts on C3H mice. All RAMT sera were shown to be free of anti-LCM activity as assayed by mouse neuat RYERSON UNIV on June 18, 2015 ebm.sagepub.com Downloaded from
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