ArticlePloS one2015
Host APOBEC3G protein inhibits HCV replication through direct binding at NS3.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Two codes of RNA editing by deamination in human diseases.Experimental & molecular medicine · 2026Review
- Association of viral RNAs in the choroid plexus with bipolar disorder and schizophrenia and evidence for the hepatitis C virus involvement in neuropathology.Translational psychiatry · 2025Article
- Tribbles pseudokinase 3 promotes enterovirus A71 infection via dual mechanisms.Emerging microbes & infections · 2024Article
- Human DNA tumor viruses evade uracil-mediated antiviral immunity.PLoS pathogens · 2023Article
- APOBEC3: Friend or Foe in Human Papillomavirus Infection and Oncogenesis?Annual review of virology · 2022Review
- Tree Shrew Cells Transduced with Human CD4 and CCR5 Support Early Steps of HIV-1 Replication, but Viral Infectivity Is Restricted by APOBEC3.Journal of virology · 2021Article
- Infection of Bronchial Epithelial Cells by the Human Adenoviruses A12, B3, and C2 Differently Regulates the Innate Antiviral Effector APOBEC3B.Journal of virology · 2021Article
- Clearing of Foreign Episomal DNA from Human Cells by CRISPRa-Mediated Activation of Cytidine Deaminases.International journal of molecular sciences · 2020Article
- Medicinal chemistry strategies toward host targeting antiviral agents.Medicinal research reviews · 2020Review
- Zika virus noncoding sfRNAs sequester multiple host-derived RNA-binding proteins and modulate mRNA decay and splicing during infection.The Journal of biological chemistry · 2019Article
- Neuralized E3 Ubiquitin Protein Ligase 3 Is an Inducible Antiviral Effector That Inhibits Hepatitis C Virus Assembly by Targeting Viral E1 Glycoprotein.Journal of virology · 2018Article
- APOBEC3G-Regulated Host Factors Interfere with Measles Virus Replication: Role of REDD1 and Mammalian TORC1 Inhibition.Journal of virology · 2018Article
- Plant-derived antivirals against hepatitis c virus infection.Virology journal · 2018Review
- TRAF6 is a novel NS3-interacting protein that inhibits classical swine fever virus replication.Scientific reports · 2017Article
- A Simple but Accurate Method for Evaluating Drug-Resistance in Infectious HCVcc System.BioMed research international · 2017Article
- CRISPR-Cas-like system in giant viruses: why MIMIVIRE is not likely to be an adaptive immune system.Virologica Sinica · 2016Article
- CD36 is a co-receptor for hepatitis C virus E1 protein attachment.Scientific reports · 2016Article
- Host restriction factors for hepatitis C virus.World journal of gastroenterology · 2016Review
- Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human APOBEC3G (hA3G) is a cytidine deaminase that restricts replication of certain viruses. We have previously reported that hA3G was a host restriction factor against hepatitis C virus (HCV) replication, and hA3G stabilizers showed a significant inhibitory activity against HCV. However, the molecular mechanism of hA3G against HCV remains unknown. We show in this study that hA3G's C-terminal directly binds HCV non-structural protein NS3 at its C-terminus, which is responsible for NS3's helicase and NTPase activity. Binding of hA3G to the C-terminus of NS3 reduced helicase activity, and therefore inhibited HCV replication. The anti-HCV mechanism of hA3G appeared to be independent of its deamination activity. Although early stage HCV infection resulted in an increase in host hA3G as an intracellular response against HCV replication, hA3G was gradually diminished after a long-term incubation, suggesting an unknown mechanism(s) that protects HCV NS3 from inactivation by hA3G. The process represents, at least partially, a cellular defensive mechanism against HCV and the action is mediated through a direct interaction between host hA3G and HCV NS3. We believe that understanding of the antiviral mechanism of hA3G against HCV might open an interesting avenue to explore hA3G stabilizers as a new class of anti-HCV agents.
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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.