Prevention of murine coxsackie B3 viral myocarditis and associated lymphoid organ atrophy with recombinant human leucocyte interferon alpha A/D.

The effects of recombinant human leucocyte interferon alpha A/D on experimental myocarditis due to coxsackie virus B3 were investigated. Specific plaque reduction assays showed that 50% of in vitro plaque formation in VERO (kidney of African green monkey) cells was inhibited by interferon alpha A/D 48 U.ml-1 when administered 24 h before infection with coxsackie virus B3. Three week old male C3H/He mice were inoculated intraperitoneally with 3 x 10(2) plaque-forming units (pfu) of coxsackie virus B3. Controls (group 1) were injected with saline. Interferon alpha A/D 10(4) (group 2) or 10(3) (group 3) U.g-1.day-1, was administered subcutaneously daily, starting 1 d before the infection. Interferon alpha A/D 10(4) U.g-1.day-1 (group 4) was also given, starting the same day. Each group consisted of ten mice. Animals were sacrificed on d 5 for evaluation. Myocardial virus titres were significantly lower in groups 2, 3, and 4 (p less than 0.05) compared with controls. Histological examination showed extensive myocardial necrosis and cellular infiltration in all untreated mice but less severe necrosis and cellular infiltration in treated groups. Thymus and spleen weights in treated groups were greater than in the untreated group, and cellular depletion was less. Thus interferon alpha A/D effectively inhibited myocardial replication of coxsackie virus B3, reduced the myocardial inflammatory response, and prevented the disease associated lymphoid organ atrophy in this animal model.