Directions for future research on the pathogenesis of arenaviral infections

The pathogenesis of arenavirus infection is considered separately for the haemorrhagic fever (HF) syndrome and for lymphocytic choriomeningitis (LCM) virus infection of rodents. Experimental models of HF have received only limited study, mainly because of the virulence of the causal agents. Two useful models (Junin virus in guinea-pigs and Machupo virus in rhesus monkeys) are now available and an attempt is made to delineate crucial questions for future studies, including the physiology of shock, disseminated intravascular coagulation, immune mediation of disease, efficacy of antibody in treatment, and relative utility of attenuated and inactivated vaccines. Immunobiologic problems currently under investigation in LCM virus infection include the mechanism of immune destruction of infected tissues, the H-2 restriction of in vitro T-cell-mediated lysis of infected target cells, the transient immunodepression that accompanies acute primary LCM virus infection, and the mechanism of T-cell-mediated clearance of virus from infected tissues following adoptive immunization of persistently infected carrier mice.