MOUSE HEPATITIS-VIRUS INFECTION OF MICE CAUSES LONG-TERM DEPLETION OFLACTATE DEHYDROGENASE-ELEVATING VIRUS-PERMISSIVE MACROPHAGES AND T-LYMPHOCYTE ALTERATIONS

Intraperitoneal injection of pathogen-free B10.A mice with mouse hepat itis virus (MHV)-A59 resulted in a short subclinical infection which w as terminated by a rapid antiviral immune response. The infection resu lted in a rapid, but transient, about 10-fold increase in the number o f macrophages and total cells in the peritoneum of the mice. This incr ease was preceded by a complete depletion of the peritoneum of the sub population of macrophages that supports a productive infection by lact ate dehydrogenase-elevating virus (LDV). The depletion of LDV-permissi ve macrophages was a long-term effect; at 50 days post-infection with MHV, the proportion of LDV-permissive macrophages in the peritoneum ha d reached only 20% of that observed in the peritoneum of uninfected mi ce, whereas the total number of macrophages in the peritoneum had retu rned to normal. Furthermore, MHV infection resulted in a long-term alt eration in the proliferative response of spleen T cells to concanavali n A (ConA) and in their ability to produce interferon gamma; several t imes higher concentrations of ConA were required to induce a maximum p roliferative response in spleen T cell populations from 5-week MHV-inf ected B10.A mice than in spleen T cell populations from infected compa nion mice but the former produced 5 times more interferon gamma than t he T cells from uninfected mice.