HIV Induces TRAIL Sensitivity in Hepatocytes |
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| Authors: | Challagundla K Babu Kanitta Suwansrinon Gary D Bren Andrew D Badley Stacey A Rizza |
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| Institution: | 1. Division of Infectious Diseases, Mayo Clinic, Rochester, Minnesota, United States of America.; 2. Program in Translational Immunovirology and Biodefense, Mayo Clinic, Rochester, Minnesota, United States of America.;New York University School of Medicine, United States of America |
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| Abstract: | BackgroundHIV infected patients have an increased susceptibility to liver disease due to Hepatitis B Virus (HBV), Hepatitis C Virus (HCV), alcoholic, and non-alcoholic steatohepatitis. Clinically, this results in limited options for antiretroviral therapy and accelerated rates of liver disease, causing liver disease to be the second leading cause of death for HIV infected patients. The mechanisms causing this propensity for liver dysfunction during HIV remains unknown.Methodology/Principal FindingsWe demonstrate that HIV and/or the HIV glycoprotein gp120 ligation of CXCR4 on hepatocytes selectively up-regulates TRAIL R2 expression and confers an acquired sensitivity to TRAIL mediated apoptosis which is mediated by JNK II, but not p38 nor G-proteins.Conclusions/SignificanceThese findings suggest that HIV infection renders hepatocytes more susceptible to liver injury during disease states associated with enhanced TRAIL production such as HBV, HCV, or steatohepatitis. |
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