Current Views on the Pathophysiology of GB Virus C Coinfection with HIV-1 Infection

GB virus C (GBV-C), a member of the Flaviviridae family of viruses, recently received considerable attention largely owing to its potential role in decelerating HIV-1 disease progression by interfering with HIV replication. With similar transmission features, GBV-C is parenterally transmitted, similar to the serum hepatitis viruses and HIV-1, and replicates in hemopoietic cells and T lymphocytes in particular, with no observable disease pathology. Progressive T-cell depletion and subsequent immune abrogation being the cardinal features of HIV-1 infection, accumulating evidence indicates that GBV-C effectively overturns HIV’s chances of exploiting the T-cell machinery and leads to enhanced survival rates of HIV-infected subjects. Much effort has been devoted to understanding the beneficial role of GBV-C in HIV disease. This review discusses recently proposed mechanisms underlying the pathophysiology of GBV-C coinfection in HIV disease.