Delayed type-hypersensitivity response of inbred strains of Syrian golden hamsters (Mesocricetus auratus) to lethal or non-lethal lymphocytic choriomeningitis virus (LCMV) infections.

In adult Syrian golden hamsters (Mesocricetus auratus), intraperitoneal or footpad inoculation of the lymphocytic choriomeningitis virus (LCMV) strains, WE or Armstrong (ARM), caused systemic infection and induced serum LCMV-antibody. Hamster and virus strain-dependent lethal disease also occurred. With WE, MHA and PD4 inbred hamsters failed to eliminate infection and died of wasting disease. LSH and CB inbred hamsters resisted lethal WE-disease and cleared infection. LVG hamsters and inbred LHC hamsters were intermediate in WE-susceptibility; some died of wasting, while others survived with little illness. Resistance to lethal WE-disease directly correlated with a delayed-type hypersensitivity (DTH) response to live-virus footpad inoculation. In WE-resistant LSH and CB hamsters, DTH-responses were induced by intraplantar WE-inoculation; footpad edema began by 5 days, reached maximum thickness by 7 to 9 days, and subsided thereafter. In the other hamster strains, DTH to WE could not be elicited. Unlike WE, ARM was hamster-avirulent; infections were self-limited and did not induce DTH. All survivors of primary LCMV (WE or ARM)-infection resisted secondary WE-challenge, and did not develop DTH to LCMV. Immunosuppressive treatments, abrogating DTH and antibody responses to LCMV, rendered all hamsters susceptible to lethal WE-infection. Hamster DTH most likely mediated resistance to virulent LCMV-infection.