Viral myocarditis is a deadly disease affecting both children and adults and causes significant morbidity and mortality. The diagnosis of this disease is often difficult and there is no effective treatment to prevent the down stream sequelae of viral myocarditis including heart failure from heart enlargement and rhythm disorder that causes sudden death. We set out in this study to develop a way to study how the virus (coxsackievirus B3) that is the most common virus responsible for this disease is able to infect human heart muscle cells and to determine whether we can develop an assay that would allow us to test candidate drugs that may be able to reduce/minimize/eliminate the ability of the virus to infect and to grow inside human heart muscle cells. We used human induced pluripotent stem cells (iPSCs) and generated heart muscle cells from these stem cells and add the virus to these cells to see what effects do the viruses have on cell’s survival and growth. We also tested the effect of a few candidate drugs that have been suggested to prevent infection of this virus, for example, interferon-beta, on the ability of the virus to grow and expand. We show that the human iPSC derived heart muscle cells express the receptor for the coxsackievirus B3 and are susceptible to being infect by them. This process simulates what does on when humans are being infected with the virus. We then down that treating of human iPSC cardiomyocytes with interferon-beta and other candidate drugs are able to reduce the level of infection by these viruses. Our study will now provide a way for drug companies and scientists to measure the ability of their lead drug candidate to protect against viral myocarditis.