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Interferons Accelerate Decay of Replication-Competent Nucleocapsids of Hepatitis B Virus
Journal article   Open access   Peer reviewed

Interferons Accelerate Decay of Replication-Competent Nucleocapsids of Hepatitis B Virus

Chunxiao Xu, Haitao Guo, Xiao-Ben Pan, Richeng Mao, Wenquan Yu, Xiaodong Xu, Lai Wei, Jinhong Chang, Timothy M. Block and Ju-Tao Guo
Journal of virology, v 84(18), pp 9332-9340
07 Jul 2010
PMID: 20610715
url
https://doi.org/10.1128/jvi.00918-10View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open
url
https://doi.org/10.1128/JVI.00918-10View
Published, Version of Record (VoR) Open

Abstract

Virus-Cell Interactions
Alpha interferon (IFN-α) is an approved medication for chronic hepatitis B. Gamma interferon (IFN-γ) is a key mediator of host antiviral immunity against hepatitis B virus (HBV) infection in vivo . However, the molecular mechanism by which these antiviral cytokines suppress HBV replication remains elusive. Using an immortalized murine hepatocyte (AML12)-derived cell line supporting tetracycline-inducible HBV replication, we show in this report that both IFN-α and IFN-γ efficiently reduce the amount of intracellular HBV nucleocapsids. Furthermore, we provide evidence suggesting that the IFN-induced cellular antiviral response is able to distinguish and selectively accelerate the decay of HBV replication-competent nucleocapsids but not empty capsids in a proteasome-dependent manner. Our findings thus reveal a novel antiviral mechanism of IFNs and provide a basis for a better understanding of HBV pathobiology.

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Collaboration types
Domestic collaboration
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Web of Science research areas
Virology
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