ArticlePLoS pathogens2010
Massive APOBEC3 editing of hepatitis B viral DNA in cirrhosis.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 160 citations in OpenAlex.
- Review
- APOBEC3B regulates HPV replication by inducing R-loop formation and DNA damage.PLoS pathogens · 2026Article
- The APOBEC3 family: a narrative review of an alternative therapeutic agent for hepatitis B virus-induced hepatocellular carcinoma.Journal of gastrointestinal oncology · 2026Review
- Hepatitis B Virus Nucleocapsid Assembly.Journal of molecular biology · 2025Review
- May I Help You with Your Coat? HIV-1 Capsid Uncoating and Reverse Transcription.International journal of molecular sciences · 2024Review
- CRISPR/Cas9-mediated base editors and their prospects for mitochondrial genome engineering.Gene therapy · 2024Review
- The Intricate Interplay between APOBEC3 Proteins and DNA Tumour Viruses.Pathogens (Basel, Switzerland) · 2024Review
- APOBEC3 deaminase editing in mpox virus as evidence for sustained human transmission since at least 2016.Science (New York, N.Y.) · 2023Article
- Monkeypox (mpox) virus: Classification, origin, transmission, genome organization, antiviral drugs, and molecular diagnosis.Journal of infection and public health · 2023Review
- An ultralong-acting tenofovir ProTide nanoformulation achieves monthslong HBV suppression.Science advances · 2022Article
- Multiple lineages of monkeypox virus detected in the United States, 2021-2022.Science (New York, N.Y.) · 2022Article
- APOBEC3: Friend or Foe in Human Papillomavirus Infection and Oncogenesis?Annual review of virology · 2022Review
- Markers of Immune Activation and Inflammation Are Associated with Higher Levels of Genetically-Intact HIV in HIV-HBV Co-Infected Individuals.Journal of virology · 2022Article
- Article
- Mutational signatures and processes in hepatobiliary cancers.Nature reviews. Gastroenterology & hepatology · 2022Review
- APOBEC3A regulates transcription from interferon-stimulated response elements.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- APOBEC3B: Future direction of liver cancer research.Frontiers in oncology · 2022Review
- Roles of APOBEC3 in hepatitis B virus (HBV) infection and hepatocarcinogenesis.Bioengineered · 2021Review
- Nature of Acquired Immune Responses, Epitope Specificity and Resultant Protection from SARS-CoV-2.Journal of personalized medicine · 2021Review
- Analysis of SARS-CoV-2 haplotypes and genomic sequences during 2020 in Victoria, Australia, in the context of putative deficits in innate immune deaminase anti-viral responses.Scandinavian journal of immunology · 2021Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA viruses, retroviruses and hepadnaviruses, such as hepatitis B virus (HBV), are vulnerable to genetic editing of single stranded DNA by host cell APOBEC3 (A3) cytidine deaminases. At least three A3 genes are up regulated by interferon-alpha in human hepatocytes while ectopic expression of activation induced deaminase (AICDA), an A3 paralog, has been noted in a variety of chronic inflammatory syndromes including hepatitis C virus infection. Yet virtually all studies of HBV editing have confined themselves to analyses of virions from culture supernatants or serum where the frequency of edited genomes is generally low (< or = 10(-2)). We decided to look at the nature and frequency of HBV editing in cirrhotic samples taken during removal of a primary hepatocellular carcinoma. Forty-one cirrhotic tissue samples (10 alcoholic, 10 HBV(+), 11 HBV(+)HCV(+) and 10 HCV(+)) as well as 4 normal livers were studied. Compared to normal liver, 5/7 APOBEC3 genes were significantly up regulated in the order: HCV+/-HBV>HBV>alcoholic cirrhosis. A3C and A3D were up regulated for all groups while the interferon inducible A3G was over expressed in virus associated cirrhosis, as was AICDA in approximately 50% of these HBV/HCV samples. While AICDA can indeed edit HBV DNA ex vivo, A3G is the dominant deaminase in vivo with up to 35% of HBV genomes being edited. Despite these highly deleterious mutant spectra, a small fraction of genomes survive and contribute to loss of HBeAg antigenemia and possibly HBsAg immune escape. In conclusion, the cytokine storm associated with chronic inflammatory responses to HBV and HCV clearly up regulates a number of A3 genes with A3G clearly being a major restriction factor for HBV. Although the mutant spectrum resulting from A3 editing is highly deleterious, a very small part, notably the lightly edited genomes, might help the virus evolve and even escape immune responses.
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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.