TLR3 and myocarditis: This hypothesis was corroborated by a study showing that myocarditis (coxsackie B virus) patients with mutant TLR-3 phenotype had increased viral replication when compared with patients with a normal TLR-3 phenotype, thus showing that genetic differences in TLR-3 together with PAR-2 modulation of INF- β effect the host’s vulnerability to viral cardiomyopathies [23,194].