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National Academy of Sciences, Proceedings of the National Academy of Sciences, 18(112), p. 5797-5802, 2015

DOI: 10.1073/pnas.1502390112

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Cellular inhibitor of apoptosis proteins prevent clearance of hepatitis B virus

Journal article published in 2015 by Gregor Ebert, Simon Preston, Cody Allison, James Cooney ORCID, Jesse G. Toe, Michael D. Stutz, Samar Ojaimi, Hamish W. Scott, Nikola Baschuk, Ueli Nachbur, Joseph Torresi, Ruth Chin, Danielle Colledge, Xin Li, Nadia Warner and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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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.