Macrophages in mice acutely infected with lymphocytic choriomeningitis virus are primed for nitric oxide synthesis.

Following infection of adult mice with lymphocytic choriomeningitis virus (LCMV) there is a well documented suppression of T-cell and B-cell functions concurrent with the strong anti-LCMV immune response. Macrophages have been shown to be infected and activated during acute LCMV infection and there is some evidence to indicate that there is altered antigen presentation in acutely infected mice. We have examined nitric oxide (NO) production by splenic macrophages during acute infection of adult mice. Our results show that these macrophages are primed for production of NO, that the inducible production of NO parallels the immune suppression, and that NO production is dependent on the presence of IFN gamma. However, neither in vivo nor in vitro treatment with N-monomethyl-L-arginine (NMA), a specific inhibitor of nitric oxide synthase, altered the induction or maintenance of virus-induced immune suppression in mice acutely infected with LCMV.