Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 112, Issue 18, Pages 5797-5802Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1502390112
Keywords
hepatitis B virus; cellular inhibitor of apoptosis proteins; cIAP1; cIAP2; TNF
Categories
Funding
- Australian Research Council Future Fellowship Award
- National Health and Medical Research Council Australia Career Development Award [637350, 541901, 541902, 1006592, 1045549, 1065626]
- Victorian State Government Operational Infrastructure Support
- Independent Research Institutes Infrastructure Support Scheme of the Australian Government National Health
- Medical Research Council
- [FT1301000166]
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Hepatitis B virus (HBV) infection can result in a spectrum of outcomes from immune-mediated control to disease progression, cirrhosis, and liver cancer. The host molecular pathways that influence and contribute to these outcomes need to be defined. Using an immuno-competent mouse model of chronic HBV infection, we identified some of the host cellular and molecular factors that impact on infection outcomes. Here, we show that cellular inhibitor of apoptosis proteins (cIAPs) attenuate TNF signaling during hepatitis B infection, and they restrict the death of infected hepatocytes, thus allowing viral persistence. Animals with a liver-specific cIAP1 and total cIAP2 deficiency efficiently control HBV infection compared with WT mice. This phenotype was partly recapitulated in mice that were deficient in cIAP2 alone. These results indicate that antagonizing the function of cIAPs may promote the clearance of HBV infection.
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