IFNA1 and myocarditis: CVB3 infection strongly activates type I interferons (IFNαs and IFNβ) and type II (IFNγ) IFN production during myocarditis to reduce viral replication via Toll-like receptor (TLR) activation including TLR3, TLR4, TLR7 and TLR9 and the transcription factor TIR domain-containing adaptor inducing interferon-β (TRIF) which is downstream of TLR3 and TLR4 [10, 47, 61–63].