Vpr protein regulates expression of cytokines associated with apopotsis

Abstract

Abstract Background: Viral protein R (Vpr) is an HIV-1 accessory protein whose function remains poorly understood. While its contribution to virus replication in dividing and non-dividing cells and to the pathogenesis of HIV-1 in many different cell types have been extensively studied. Recently, HIV-1 viral protein R (Vpr) has been demonstrated to induce host cell G2 / M phase and apoptosis in infected cells. However, its precise mechanism of apoptosis nevertheless remains enigmatic. Methods: In this study, we established overexpression and silencing of HIV-1 Vpr gene in 293T and Jurkat cells to investigate the relationship among HIV-1 Vpr with IL-17A, IFN-γ and c-IAP2 expression. Results: The results demonstrated that overexpression of HIV-1 Vpr gene significantly decreased IL-17A, IFN-γ concentration as well as c-IAP2 expression and induced apoptosis in Jurkat cells, but not in 293T stable cells. Meanwhile, silencing of Vprgene expression reversed the effects of Vpr on IL-17A, IFN-γ, and c-IAP2 expression, and apoptosis in Jurkat cells. Conclusion: HIV-1 Vpr negatively regulates IL-17A, IFN-γ, and c-IAP2 expression and induce apoptosis in T lymphocytes.