Thus, IL-4 absence in acute phase of experimental infection with <i>T. cruzi</i> Colombian strain reduces myocarditis due to lower IFN-<i>γ</i> production and greater IL-10 production <i>in situ</i> and this pattern is not influenced by splenocyte general repertoire.
The reovirus M1 gene-encoded μ2 protein is a strain-specific repressor of IFN-β signaling, providing one possible mechanism for the variation in resistance to IFN and induction of myocarditis between different reovirus strains.