ArticleScientific reports2017
Hepatitis B virus X protein is capable of down-regulating protein level of host antiviral protein APOBEC3G.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The trial behind it
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Analysis of the APOBEC3 footprint across the Anelloviridae family.Archives of virology · 2026Article
- Exosomal nanocarriers of immune fate: molecular insights into cancer immunity, pathogen defense, and emerging immunotherapies.Clinical and experimental immunology · 2026Review
- Exosomes target HBV-host interactions to remodel the hepatic immune microenvironment.Journal of nanobiotechnology · 2024Review
- Human DNA tumor viruses evade uracil-mediated antiviral immunity.PLoS pathogens · 2023Article
- Many Ways to Communicate-Crosstalk between the HBV-Infected Cell and Its Environment.Pathogens (Basel, Switzerland) · 2022Review
- APOBEC3: Friend or Foe in Human Papillomavirus Infection and Oncogenesis?Annual review of virology · 2022Review
- Inhibition of base editors with anti-deaminases derived from viruses.Nature communications · 2022Article
- A Comprehensive Insight into the Role of Exosomes in Viral Infection: Dual Faces Bearing Different Functions.Pharmaceutics · 2021Review
- Emerging role and therapeutic application of exosome in hepatitis virus infection and associated diseases.Journal of gastroenterology · 2021Review
- The Role of Viral Proteins in the Regulation of Exosomes Biogenesis.Frontiers in cellular and infection microbiology · 2021Review
- Article
- The Role of APOBECs in Viral Replication.Microorganisms · 2020Review
- Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants.Frontiers in microbiology · 2020Article
- Targeting Hepatitis B Virus Covalently Closed Circular DNA and Hepatitis B Virus X Protein: Recent Advances and New Approaches.ACS infectious diseases · 2019Article
- Exosomal Interferon-Induced Transmembrane Protein 2 Transmitted to Dendritic Cells Inhibits Interferon Alpha Pathway Activation and Blocks Anti-Hepatitis B Virus Efficacy of Exogenous Interferon Alpha.Hepatology (Baltimore, Md.) · 2019Article
- From APOBEC to ZAP: Diverse mechanisms used by cellular restriction factors to inhibit virus infections.Biochimica et biophysica acta. Molecular cell research · 2019Review
- Exosomes Modulate the Viral Replication and Host Immune Responses in HBV Infection.BioMed research international · 2019Review
- Role of HBx in hepatitis B virus persistence and its therapeutic implications.Current opinion in virology · 2018Review
- Asymmetric Modification of Hepatitis B Virus (HBV) Genomes by an Endogenous Cytidine Deaminase inside HBV Cores Informs a Model of Reverse Transcription.Journal of virology · 2018Article
- Exosomes in Pathogen Infections: A Bridge to Deliver Molecules and Link Functions.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The apolipoprotein B mRNA editing catalytic polypeptide-like (APOBEC) family proteins bind RNA and single-stranded DNA, and create C-to-U base modifications through cytidine deaminase activity. APOBEC3G restricts human immunodeficiency virus 1 (HIV-1) infection by creating hypermutations in proviral DNA, while HIV-1-encoded vif protein antagonizes such restriction by targeting APOBEC3G for degradation. APOBEC3G also inhibits hepatitis B virus (HBV): APOBEC3G co-expression inhibits HBV replication and evidences exist indicating APOBEC3G-mediated HBV hypermutations in patients. HBV encodes a small non-structural X protein (HBx) with a recognized activating effect on HBV life cycle. In this work, we report the discovery that HBx selectively and dose-dependently decreases the protein level of co-expressed APOBEC3G in transfected Huh-7 cells. The effect was shown to take place post-translationally, but does not rely on protein degradation via proteasome or lysosome. Further work demonstrated that intracellular APOBEC3G is normally exported via exosome secretion and inhibition of exosome biogenesis causes retention of intracellular APOBEC3G. Finally, HBx co-expression specifically enhanced externalization of APOBEC3G via exosomes, resulting in decrease of intracellular APOBEC3G protein level. These data suggest the possibility that in addition to other mechanisms, HBx-mediated activation of HBV might also involve antagonizing of intracellular restriction factor APOBEC3G through promotion of its export.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.