Infection with the lactate dehydrogenase-elevating virus (LDV) triggers a generally fatal paralytic disease in old immunosuppressed C58 mice, but not in comparable mice of many other strains. We have compared the replication of LDV and the humoral immune response to it in C58 mice and mice of various resistant strains. Plasma LDV titres of persistently infected C58 mice were about tenfold higher than in other strains of mice and the proportion of LDV-permissive macrophages in peritoneal exudates of C58 mice was about twice as high as that observed in other mouse strains. C58 mice developed normal levels of anti-LDV IgG, as measured by ELISA, and normal levels of IgG that sensitized LDV to neutralization by rabbit anti-mouse IgG. C58 mice also developed normal IgM and IgG responses to human γ-globulin and sheep erythrocytes. The antibody responses to LDV were similarly inhibited by cyclophosphamide in C58 and resistent strains of mice, which enhanced the incidence of signs of paralysis only in C58 mice. Thus, the sensitivity of C58 mice to LDV-induced paralytic disease is not due to an inherent inability of the mice to mount a humoral antibody response to LDV, and a suppression of the antibody response by cyclophosphamide is not the only prerequisite for development of the disease. We have quantified LDV in various tissues of immunosuppressed and non-immunosuppressed, 8- or 9-month-old C58 mice as a function of time after LDV infection and in relation to the development of paralytic disease. Changes in tissue LDV titres as a function of time after infection paralleled those found in the plasma; LDV titres were highest 1 day post-infection, and then decreased to a lower persistent level during the next 1 to 2 weeks. Tissue LDV titres, including those of the spinal cord, were lower than those in the plasma, and our results indicate that most of the LDV in tissue homogenates may be attributable to blood contamination, even though the animals were extensively perfused before removal of the tissues.


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