ReviewViruses2017
Hepatitis B Virus and DNA Damage Response: Interactions and Consequences for the Infection.
Review in Viruses, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Review
- Conserved recombination patterns across hepatitis B genotypes: a retrospective study.Virology journal · 2025Article
- Caffeine restricts hepatitis B virus transcription by inhibitingFrontiers in microbiology · 2025Article
- Regulation of R-Loops in DNA Tumor Viruses.Pathogens (Basel, Switzerland) · 2024Review
- The oncogenic role of hepatitis B virus X gene in hepatocarcinogenesis: recent updates.Exploration of targeted anti-tumor therapy · 2024Review
- Exploring the Microbiome in Gastric Cancer: Assessing Potential Implications and Contextualizing Microorganisms beyondCancers · 2023Review
- Targeting DNA repair to enhance the efficacy of sorafenib in hepatocellular carcinoma.Journal of cellular biochemistry · 2022Article
- Review
- Review
- Reactive Oxygen Species Bridge the Gap between Chronic Inflammation and Tumor Development.Oxidative medicine and cellular longevity · 2022Review
- Network pharmacology andFrontiers in pharmacology · 2022Article
- PRCC reduces the sensitivity of cancer cells to DNA damage by inhibiting JNK and ATM/ATR pathways and results in a poor prognosis in hepatocellular carcinoma.Cell & bioscience · 2021Article
- Aberrant Splicing Events and Epigenetics in Viral Oncogenomics: Current Therapeutic Strategies.Cells · 2021Review
- Liver Cirrhosis in Chronic Hepatitis B Patients Is Associated with Genetic Variations in DNA Repair Pathway Genes.Cancers · 2020Article
- Chronic inflammation: key player and biomarker-set to predict and prevent cancer development and progression based on individualized patient profiles.The EPMA journal · 2019Review
- ATM and ATR Expression Potentiates HBV Replication and Contributes to Reactivation of HBV Infection upon DNA Damage.Viruses · 2019Article
- Intertwined: SAMHD1 cellular functions, restriction, and viral evasion strategies.Medical microbiology and immunology · 2019Review
- Virological Basis for the Cure of Chronic Hepatitis B.ACS infectious diseases · 2019Review
- Behaviors and Attitudes of Polish Health Care Workers with Respect to the Hazards from Blood-Borne Pathogens: A Questionnaire-Based Study.International journal of environmental research and public health · 2019Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) is a major etiologic agent of acute and chronic hepatitis, and end-stage liver disease. Establishment of HBV infection, progression to persistency and pathogenesis are determined by viral and cellular factors, some of which remain still undefined. Key steps of HBV life cycle e.g., transformation of genomic viral DNA into transcriptionally active episomal DNA (cccDNA) or transcription of viral mRNAs from cccDNA, take place in the nucleus of infected cells and strongly depend on enzymatic activities provided by cellular proteins. In this regard, DNA damage response (DDR) pathways and some DDR proteins are being recognized as important factors regulating the infection. On one hand, HBV highjacks specific DDR proteins to successfully complete some of the steps of its life cycle. On the other hand, HBV subverts DDR pathways to presumably create a cellular environment that favours its replication. Direct consequences of these interactions are: HBV DNA integration into host chromosomal DNA, and accumulation of mutations in host chromosomal DNA that could eventually trigger carcinogenic processes, which would explain in part the incidence of hepatocellular carcinoma in chronically infected patients. Unravelling the interactions that HBV establishes with DDR pathways might help identify new molecular targets for therapeutic intervention.
Indexed as
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What OpenQuestion holds
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.