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Title: Cellular inhibitor of apoptosis proteins prevent clearance of hepatitis B virus.
Austin Authors: Ebert, Gregor;Preston, Simon;Allison, Cody;Cooney, James;Toe, Jesse G;Stutz, Michael D;Ojaimi, Samar;Scott, Hamish W;Baschuk, Nikola;Nachbur, Ueli;Torresi, Joseph ;Chin, Ruth;Colledge, Danielle;Li, Xin;Warner, Nadia;Revill, Peter;Bowden, Scott;Silke, John;Begley, C Glenn;Pellegrini, Marc
Affiliation: Division of Infection and Immunity and Cell Signaling and Cell Death, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia
Faculty of Science Technology and Engineering, School of Molecular Sciences, Department of Biochemistry, LaTrobe Institute for Molecular Science, Bundoora, VIC 3086, Australia
Department of Infectious Diseases and Department of Medicine, Austin Hospital, The University of Melbourne, Heidelberg, VIC 3084, Australia
Division of Molecular Research and Development, Victorian Infectious Diseases Reference Laboratory, Peter Doherty Institute, Melbourne, VIC 3000, Australia
Department of Medical Biology, The University of Melbourne, Parkville, VIC 3010, Australia
Research and Development Division, TetraLogic Pharmaceuticals Corporation, Inc., Malvern, PA 19355.
Issue Date: 20-Apr-2015
Publication information: Proceedings of the National Academy of Sciences of the United States of America 2015; 112(18): 5797-802
Abstract: 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 immunocompetent 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.
Gov't Doc #: 25902529
DOI: 10.1073/pnas.1502390112
Type: Journal Article
Subjects: TNF
cellular inhibitor of apoptosis proteins
hepatitis B virus
Appears in Collections:Journal articles

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