Journal
EMERGING MICROBES & INFECTIONS
Volume 9, Issue 1, Pages 366-377Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/22221751.2020.1725398
Keywords
Hepatitis B virus; APOBEC3B; DHX9; interaction; attenuate
Categories
Funding
- National Key Research and Development Project [2018YFE0107500]
- National Sciences Foundation of China [81661148057, NSFC 81471945]
- Natural Science Foundation Project of CQ CSTC [cstc2018jcyjAX0166]
- National Science and Technology Major Project from Science & Technology Commission of China [2017ZX10202203]
- Program for Innovation Team of Higher Education in Chongqing [CXTDX201601015]
- Scientific Research Innovation Project for Postgraduate in Chongqing [CYB18163]
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Hepatitis B virus (HBV) is a partially double-stranded DNA virus that replicates by reverse transcription. We previously demonstrated that the host restriction factor-APOBEC3B (A3B) inhibited HBV replication which was dependent on its deaminase activity during reverse transcription. However, the host factors involved in the process of regulating the anti-HBV function of A3B are less known. In this research, to obtain a comprehensive understanding of the interaction networks of A3B, we conducted coimmunoprecipitation and mass spectrometry to identify A3B-interacting proteins in the presence of HBV. By this approach, we determined that DExD/H-box helicase 9 (DHX9) suppressed the anti-HBV effect of A3B, and this suppression was dependent on their interaction. Although DHX9 did not affect the deamination activity of A3B in vitro assay or the viral DNA editing of A3B in HepG2-NTCP cells that support HBV infection, it inhibited the binding of A3B with pgRNA. These data suggest that DHX9 can interact with A3B and attenuate the anti-HBV efficacy of A3B.
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