Related Experiment Video
Updated: Jun 25, 2026
10:12
Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis
Published on: September 11, 2019
HIV induces TRAIL sensitivity in hepatocytes.
Challagundla K Babu1, Kanitta Suwansrinon, Gary D Bren
1Division of Infectious Diseases, Mayo Clinic, Rochester, Minnesota, United States of America.
Plos One
|February 28, 2009
Summary
HIV infection increases liver injury risk in patients by making liver cells, or hepatocytes, more sensitive to TRAIL-mediated apoptosis. This heightened susceptibility is linked to conditions like Hepatitis B and C.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- HIV-infected individuals face higher risks of liver disease from viral hepatitis (HBV, HCV), alcohol, and steatohepatitis.
- Liver disease is the second leading cause of death in HIV patients, with limited treatment options.
- The underlying mechanisms of HIV-associated liver dysfunction remain unclear.
Purpose of the Study:
- To investigate how HIV infection impacts hepatocyte susceptibility to liver injury.
- To elucidate the molecular mechanisms behind HIV-induced liver dysfunction.
Main Methods:
- Examined the effect of HIV and its glycoprotein gp120 on hepatocyte apoptosis.
- Investigated the role of CXCR4, TRAIL R2, JNK II, p38, and G-proteins in HIV-mediated hepatocyte apoptosis.
Main Results:
- HIV and/or gp120 binding to CXCR4 on hepatocytes up-regulates TRAIL R2 expression.
- This up-regulation confers acquired sensitivity to TRAIL-mediated apoptosis.
- The apoptosis pathway is mediated by JNK II, independent of p38 and G-proteins.
Conclusions:
- HIV infection sensitizes hepatocytes to apoptosis induced by Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL).
- This increased susceptibility contributes to liver injury in conditions with elevated TRAIL, such as HBV, HCV, and steatohepatitis.
