These observations and our bioinformatics analyses of differentially regulated proteins not only validate our hypothesis that HIV induces unique (fetal) genes MYH6 and MYH7 in chronically infected T-cells, but also demonstrate that the upregulation of both MYH6 (alpha MHC) and MYH7 (beta MHC) in HIV-infected cells causes an overabundance of Ca2 + and ATPase in the heart muscles, accounting for the cardiac stress and heart failure, particularly in patients whose hearts may be infiltrated with HIV-infected T-cells. The gene discussed is MYH6; the disease is heart failure.