Effect of interferon on exogenous, endogenous, and chronic murine leukemia virus infection

Abstract

Abstract The effect of purified mouse interferon on the replication of AKR mouse leukemia virus (MLV) in a clonal line of AKR cells was studied, with emphasis on comparing the effect of interferon on the replication of exogenous virus, activation of endogenous virus by IdUrd, and production of virus by chronically infected cells. It was found that interferon inhibited replication of virus in all three systems. Interferon did not abort exogenous infection or virus induction by IdUrd, but only delayed appearance of infectious virus. Virus production by chronically infected cells also was suppressed in the presence of interferon; however, after removal of interferon, rapid recovery of virus production occurred. Under conditions where interferon treatment inhibited virus yield as measured both by infectious virus and virion-associated reverse transcriptase activity, no significant inhibition of synthesis of virus specific (gs) antigen was observed (as measured by immunofluorescence and radioimmunoassay for p30 protein). These results indicate that unlike its effect on the majority of viruses, interferon does not inhibit MLV by a general inhibition of viral protein synthesis; rather, it appears to inhibit one or more of the later steps in MLV replication which occur after the expression of viral gs antigen. The interferon block of acute exogenous or IdUrd-induced endogenous infection appeared to occur prior to virus assembly, resulting in a marked decrease in the number of free and cell-associated particles. In the chronic infection, however, the interferon treatment only partially prevented assembly and release of virus particles, but these had markedly reduced infectivity.