Journal article
Interferons Accelerate Decay of Replication-Competent Nucleocapsids of Hepatitis B Virus
Journal of virology, Vol.84(18), pp.9332-9340
07 Jul 2010
PMCID: PMC2937652
PMID: 20610715
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
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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Details
- Title
- Interferons Accelerate Decay of Replication-Competent Nucleocapsids of Hepatitis B Virus
- Creators
- Chunxiao Xu - Drexel UniversityHaitao Guo - Drexel UniversityXiao-Ben Pan - Drexel UniversityRicheng Mao - Drexel UniversityWenquan Yu - Hepatitis B FoundationXiaodong Xu - Hepatitis B FoundationLai Wei - Peking University People's HospitalJinhong Chang - Drexel UniversityTimothy M. Block - Drexel UniversityJu-Tao Guo - Drexel University
- Publication Details
- Journal of virology, Vol.84(18), pp.9332-9340
- Publisher
- American Society for Microbiology (ASM)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Microbiology and Immunology
- Identifiers
- 991019167592604721
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- Domestic collaboration
- International collaboration
- Web of Science research areas
- Virology