Immunodepressive Effect of Rauscher Leukemia Virus on Antinuclear Antibody Formation in New Zealand Black Mice 1,2

8-day-old New Zealand Black (NZB) strain mice resulted in erythro-leukemogenesis accompanied by anemia and hepatosplenomegaly. The diminution in antinuclear antibody (ANA) Formation was directly related to the dose of virus administered. Virus-inFected animals that survived eventually developed ANA responses comparable to, but not exceeding, those of the controls. InFection of ANA-positive NZB mice at 1.5, 5, and 12 months of age resulted in leukemia development unassociated with any significant reversal of strongly positive reactions. ANA reactivity was not precipitated in the normally negative BALB/c or C57BL/6 strains after RLV inoculation.-J Nat Cancer Inst 48: 159-163, 1972. RAU SCHER leukemia virus (RLV) infection of New Zealand Black (NZB) mice depressed pri-mary and secondary antibody responses after sheep erythrocyte immunization and delayed the onset and incidence of positive Coombs ' reactivity (1). However, the formation of antinuclear antibodies (ANA) was accelerated in New Zealand (NZ) mice by chronic infection with polyoma and lymphoctyic choriomeningitis (LCM) viruses (2). Also, infection of NZ mice with Moloney leukemia virus has led to enhanced anti-RNA antibody production (3). These findings have suggested that viruses may act as antigenic stimuli or that viral infection may result in nonspecific release of host nuclear antigens. The present investigation evaluates the influence of RLV infection on the development of ANA. A sensitive indirect immunofluorescence technique (4) made possible the detection of ANA in the plasma of NZB mice before they reached 1 month of age