We have studied the effects of LP-BM5 MuLV-induced murine acquired immunodeficiency syndrome (MAIDS) on concomitant murine cytomegalovirus (MCMV) infection in the livers of C57BL mice. A delayed inflammatory response in livers of mice with MAIDS (M(+)) on day 4 was associated with impaired clearance of MCMV-infected cells 6 days after infection. This correlated with increased levels of inflammation and serum alanine transaminase. The latter reflects enhanced hepatic necrosis, which was evident histologically. Delayed-type hypersensitivity responses to MCMV antigen were unimpaired in M(+) mice and were mediated by CD8(+) cells. Depletion of NK1.1(+) cells from M(+) mice increased MCMV replication and associated liver damage on day 6, whereas CD8(+) depletion had little effect. In contrast, in the presence of CD8(+) cells M(-) C57BL mice did not require NK1.1(+) cells from control of hepatic MCMV infection, but dual NK1.1(+) and CD8(+) depletion dramatically potentiated hepatic MCMV replication. Our results suggest that M(+) mice may acquire non-NK1.1(+) and non-CD8(+) cells that are able to partially control hepatic MCMV infection. These findings are discussed with reference to mortality in M(+) mice after high-dose MCMV infection, as this is initially delayed but ultimately higher than in M(-) controls.
|Journal||American Journal of Pathology|
|Publication status||Published - 1997|