DHX9 interacts with APOBEC3B and attenuates the anti-HBV effect of APOBEC3B
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 hos...
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Taylor & Francis Group
2020-01-01
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| Series: | Emerging Microbes and Infections |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/22221751.2020.1725398 |
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| author | Yanmeng Chen Bocun Shen Xiaochuan Zheng Quanxin Long Jie Xia Yao Huang Xuefei Cai Deqiang Wang Juan Chen Ni Tang Ailong Huang Yuan Hu |
| author_facet | Yanmeng Chen Bocun Shen Xiaochuan Zheng Quanxin Long Jie Xia Yao Huang Xuefei Cai Deqiang Wang Juan Chen Ni Tang Ailong Huang Yuan Hu |
| author_sort | Yanmeng Chen |
| collection | DOAJ |
| description | 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.Abbreviations: 3D-PCR: differential DNA denaturation PCR; APOBEC3: apolipoprotein B mRNA-editing catalytic polypeptide 3; cccDNA: covalently closed circular DNA; co-IP: coimmunoprecipitation; DDX: DExD-box RNA helicases; HBc: HBV core protein; HBV: hepatitis B virus; HepAD38: HepG2 cell line stably transfected with HBV DNA; HepG2-NTCP: HepG2 cell line stably transfected with Na+/taurocholate cotransporter polypeptide; Huh7: human hepatoma cell line; pgRNA: pregenomic RNA; PPI: protein–protein interactions; RC DNA: relaxed circular DNA. |
| format | Article |
| id | doaj-art-3c2c19292d6948d381b47b30b44dee2c |
| institution | OA Journals |
| issn | 2222-1751 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Emerging Microbes and Infections |
| spelling | doaj-art-3c2c19292d6948d381b47b30b44dee2c2025-08-20T02:12:20ZengTaylor & Francis GroupEmerging Microbes and Infections2222-17512020-01-019136637710.1080/22221751.2020.1725398DHX9 interacts with APOBEC3B and attenuates the anti-HBV effect of APOBEC3BYanmeng Chen0Bocun Shen1Xiaochuan Zheng2Quanxin Long3Jie Xia4Yao Huang5Xuefei Cai6Deqiang Wang7Juan Chen8Ni Tang9Ailong Huang10Yuan Hu11Key Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaKey Laboratory of Molecular Biology on Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, People’s Republic of ChinaHepatitis 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.Abbreviations: 3D-PCR: differential DNA denaturation PCR; APOBEC3: apolipoprotein B mRNA-editing catalytic polypeptide 3; cccDNA: covalently closed circular DNA; co-IP: coimmunoprecipitation; DDX: DExD-box RNA helicases; HBc: HBV core protein; HBV: hepatitis B virus; HepAD38: HepG2 cell line stably transfected with HBV DNA; HepG2-NTCP: HepG2 cell line stably transfected with Na+/taurocholate cotransporter polypeptide; Huh7: human hepatoma cell line; pgRNA: pregenomic RNA; PPI: protein–protein interactions; RC DNA: relaxed circular DNA.https://www.tandfonline.com/doi/10.1080/22221751.2020.1725398Hepatitis B virusAPOBEC3BDHX9interactionattenuate |
| spellingShingle | Yanmeng Chen Bocun Shen Xiaochuan Zheng Quanxin Long Jie Xia Yao Huang Xuefei Cai Deqiang Wang Juan Chen Ni Tang Ailong Huang Yuan Hu DHX9 interacts with APOBEC3B and attenuates the anti-HBV effect of APOBEC3B Emerging Microbes and Infections Hepatitis B virus APOBEC3B DHX9 interaction attenuate |
| title | DHX9 interacts with APOBEC3B and attenuates the anti-HBV effect of APOBEC3B |
| title_full | DHX9 interacts with APOBEC3B and attenuates the anti-HBV effect of APOBEC3B |
| title_fullStr | DHX9 interacts with APOBEC3B and attenuates the anti-HBV effect of APOBEC3B |
| title_full_unstemmed | DHX9 interacts with APOBEC3B and attenuates the anti-HBV effect of APOBEC3B |
| title_short | DHX9 interacts with APOBEC3B and attenuates the anti-HBV effect of APOBEC3B |
| title_sort | dhx9 interacts with apobec3b and attenuates the anti hbv effect of apobec3b |
| topic | Hepatitis B virus APOBEC3B DHX9 interaction attenuate |
| url | https://www.tandfonline.com/doi/10.1080/22221751.2020.1725398 |
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