Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12756
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dc.contributor.authorEbert, Gregoren
dc.contributor.authorPreston, Simonen
dc.contributor.authorAllison, Codyen
dc.contributor.authorCooney, Jamesen
dc.contributor.authorToe, Jesse Gen
dc.contributor.authorStutz, Michael Den
dc.contributor.authorOjaimi, Samaren
dc.contributor.authorScott, Hamish Wen
dc.contributor.authorBaschuk, Nikolaen
dc.contributor.authorNachbur, Uelien
dc.contributor.authorTorresi, Josephen
dc.contributor.authorChin, Ruthen
dc.contributor.authorColledge, Danielleen
dc.contributor.authorLi, Xinen
dc.contributor.authorWarner, Nadiaen
dc.contributor.authorRevill, Peteren
dc.contributor.authorBowden, Scotten
dc.contributor.authorSilke, Johnen
dc.contributor.authorBegley, C Glennen
dc.contributor.authorPellegrini, Marcen
dc.date.accessioned2015-05-16T02:29:38Z
dc.date.available2015-05-16T02:29:38Z
dc.date.issued2015-04-20en
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America 2015; 112(18): 5797-802en
dc.identifier.govdoc25902529en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/12756en
dc.description.abstractHepatitis 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.en
dc.language.isoenen
dc.subject.otherTNFen
dc.subject.othercIAP1en
dc.subject.othercIAP2en
dc.subject.othercellular inhibitor of apoptosis proteinsen
dc.subject.otherhepatitis B virusen
dc.titleCellular inhibitor of apoptosis proteins prevent clearance of hepatitis B virus.en
dc.typeJournal Articleen
dc.identifier.journaltitleProceedings of the National Academy of Sciences of the United States of Americaen
dc.identifier.affiliationDivision of Infection and Immunity and Cell Signaling and Cell Death, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australiaen
dc.identifier.affiliationFaculty of Science Technology and Engineering, School of Molecular Sciences, Department of Biochemistry, LaTrobe Institute for Molecular Science, Bundoora, VIC 3086, Australiaen
dc.identifier.affiliationDepartment of Infectious Diseases and Department of Medicine, Austin Hospital, The University of Melbourne, Heidelberg, VIC 3084, Australiaen
dc.identifier.affiliationDivision of Molecular Research and Development, Victorian Infectious Diseases Reference Laboratory, Peter Doherty Institute, Melbourne, VIC 3000, Australiaen
dc.identifier.affiliationDepartment of Medical Biology, The University of Melbourne, Parkville, VIC 3010, Australiaen
dc.identifier.affiliationResearch and Development Division, TetraLogic Pharmaceuticals Corporation, Inc., Malvern, PA 19355.en
dc.identifier.doi10.1073/pnas.1502390112en
dc.description.pages5797-802en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/25902529en
dc.type.austinJournal Articleen
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