The role of interferon regulatory factors in the cardiac response to viral infection

Reovirus-induced murine myocarditis provides an excellent model for the human disease. Cardiac tissue damage varies between reovirus strains, and is caused by a direct viral cytopathogenic effect. One determinant of virus-induced cardiac tissue damage is the cardiac interferon-beta (IFN-beta) response to viral infection. Nonmyocarditic reoviruses induce more IFN-beta and/or are more sensitive to the antiviral effects of IFN-beta in cardiac cells than myocarditis reoviruses. The roles of interferon regulatory factors (IRFs) in the cardiac response to viral infection are reviewed, and results suggest possible cardiac-specific variations in IRF-3 and IRF-1 function. In addition, data are presented indicating that the role of IRF-2 in regulation of IFN-beta expression is cell type-specific and differs between skeletal and cardiac muscle cells. Together, results suggest that the heart may provide a unique environment for IRF function, critical for protection against virus-induced cardiac damage.