Relationship of the Anti-lymphocytic Choriomeningitis Immune Response to Tissue Injury in Chronic Lymphocytic Choriomeningitis

The possibility of an immunologic basis for the tissue injury associated with persistent lymphocytic choriomeningitis (LCM) 1 viral infection in mice is suggested by several pieces of evidence. First, chronic LCM infection per se usually is not associated with cytopathogenicity. Mice persistently infected with LCM (LCM carriers) of most strains demonstrate high titers of virus in virtally all tissues and yet most of these tissues show little, if any, evidence of cellular injury (1-6). Also, LCM infection of a variety of cells in tissue culture is usually not accompanied by cell injury despite active viral replication (7-10). Second, adult mice inoculated with LCM virus develop an acute fatal disease only when they make an anti-LCM response. In such adult infections, immunosuppression, by several methods, prevents acute disease (11-15). The LCM carrier state develops in mice inoculated with LCM virus shortly after birth (5, 16, 17) or infected transplacentally in utero (18). Such chronically infected mice carry high titers of virus in blood and organs and apparently make an anti-LCM antibody response throughout their life (6, 19). LCM carrier mice of several strains develop an associated chronic disease. Those strains carrying the largest amount of LCM virus and apparently making the greatest antiLCM antibody response develop the earliest and most severe disease.