In the case of experimental animals, which had no responses, Th1 mediated and Th17 (IL17A−/− IFNγ−/−), virus-initiated development of myocarditis was accompanied by activation of Th2 cells and the development of eosinophilic myocarditis, clinically similar to human myocarditis [95]. The gene discussed is IFNG; the disease is myocarditis.