Although the majority of mouse strains infected with lactate dehydrogenase-elevating virus (LDV) do not show any particular symptoms, the virus is able to induce acute poliomyelitis in C58 or AKR mice. Murine leukaemia virus (MuLV) has been detected at a high titre in the spinal cord of affected mice. In this study, we have analysed the possible role of MuLV in the induction of neurological disease by LDV. Immunofluorescent staining, autoradiography and an infectivity assay of virus yield have shown that LDV replicated in continuous mouse and rat cell lines that had been infected with an ecotropic MuLV isolated from C58 mice, but did not replicate in cells not infected with MuLV. No significant differences in infection were observed among the various ecotropic MuLVs employed, except for Friend leukaemia virus which rendered the cells susceptible to LDV least efficiently. The infectivity of the neurovirulent strain, LDV-C, to MuLV-infected cells was 50- to 100-fold greater than that of the avirulent strains (LDV-N, -Nu, -R and -P). The infectivity to macrophages was almost the same for virulent and avirulent strains. Adsorption studies using a radiolabelled virus revealed that LDV-C was adsorbed to MuLV-infected cells more efficiently than the avirulent strain, LDV-N. The difference in infectivity to these cells, therefore, may be due in part to the difference in adsorption rate. This may suggest differences in the interaction of the viral proteins with MuLV-infected cells from those with macrophages at the initiation of virus infection. These results may be relevant to the mechanisms of paralytic disease caused by LDV infection in C58 mice.


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