Lactate dehydrogenase-elevating virus induces anti-Golgi apparatus antibodies.

A recently described autoantibody-inducing agent in mice was further characterized. Tentatively designated AGIA (anti-Golgi apparatus-inducing agent), this agent has previously been shown to cause antibody production against Golgi apparatus (GA) antigen of cells from different vertebrate species as well as against tumour surface antigen of the Moloney murine sarcoma virus-non-producer transformant Sac. It was shown to possess the properties characteristic of lactate dehydrogenase-elevating virus (LDV). It induced elevation of lactate dehydrogenase levels in the blood, persistent lifelong viraemia in mice and serum titres of up to 10(11) infectious doses (ID50) per ml in the acute phase of infection. Its replication in vitro was limited to subpopulations of murine peritoneal macrophages. Electron microscopy of AGIA-infected macrophages and of serum of infected mice revealed virus-like particles with a morphology resembling LDV. The buoyant density of AGIA was approximately 1.14 g/ml. Both the enzyme-elevating activity and the autoantibody-inducing activity were shown to belong to LDV. Infection of STU mice with two established strains of LDV (LDVROW and LDVPLA) was also found to induce both autoantibody groups. In both cases, after infection with AGIA as well as after infection with the two known LDV isolates, anti-Sac cell antibodies occurred at comparable titres. However, anti-GA antibody titres were rather low after infection with LDVROW and LDVPLA compared with AGIA infection. Serological cross-reactivity was demonstrated between AGIA-, LDVROW- and LDVPLA-infected macrophages. AGIA induced anti-GA antibodies in all six mouse strains tested (STU, DBA/2, BALB/c, C3H/He, NMRI, C57BL/6); however, anti-Sac cell antibodies did not develop in C57BL/6 mice.