They found that the severity of myocarditis, degree of viral replication, and levels of IL-1β/IL-18 expression were significantly reduced in TLR4-deficient mice and that TLR4 as well as IL-12Rβ1 aggravated CVB3 infection and myocarditis but IFN-γ inhibited viral replication. Here, IFNG is linked to myocarditis.