ReviewViruses2020
Interplay between Hepatitis D Virus and the Interferon Response.
Review in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 30 citations in OpenAlex.
- The Impact of Chronic Hepatitis D Virus Infection on Health-Related Quality of Life and Fatigue: A Real-World International Study.Journal of viral hepatitis · 2026Article
- Double trouble: how co- and superinfections shape viral dynamics and host responses.Journal of virology · 2026Review
- Woodchuck and deer Hepatitis Delta-like agents show distinct innate immune activation and IFN-resistance compared to human Hepatitis D Virus.Scientific reports · 2026Article
- Hepatitis B virus and hepatitis D virus co-infection complicated by autoimmune hepatitis: Two case reports.World journal of clinical cases · 2025Article
- Host Immune Response in Chronic Hepatitis Delta: Implications for Pathogenesis and Therapy.Pathogens (Basel, Switzerland) · 2025Review
- Hepatitis Delta Virus and Hepatocellular Carcinoma.Pathogens (Basel, Switzerland) · 2024Review
- Interferon-Free Regimens and Direct-Acting Antiviral Agents for Delta Hepatitis: Are We There Yet?Current issues in molecular biology · 2023Review
- Hepatitis B and Hepatitis D Viruses: A Comprehensive Update with an Immunological Focus.International journal of molecular sciences · 2022Review
- Review
- [Viral hepatitis A to E: prevalence, pathogen characteristics, and pathogenesis].Bundesgesundheitsblatt, Gesundheitsforschung, Gesundheitsschutz · 2022Review
- Adaptive Immune Responses, Immune Escape and Immune-Mediated Pathogenesis during HDV Infection.Viruses · 2022Review
- Multiple Regions Drive Hepatitis Delta Virus Proliferation and Are Therapeutic Targets.Frontiers in microbiology · 2022Review
- Low prevalence of hepatitis delta infection in Cuban HBsAg carriers: Prospect for elimination.Frontiers in medicine · 2022Article
- NLRX1 can counteract innate immune response induced by an external stimulus favoring HBV infection by competitive inhibition of MAVS-RLRs signaling in HepG2-NTCP cells.Science progress · 2021Article
- Human hepatitis D virus-specific T cell epitopes.JHEP reports : innovation in hepatology · 2021Review
- Innate immunity in hepatitis B and D virus infection: consequences for viral persistence, inflammation, and T cell recognition.Seminars in immunopathology · 2021Review
- Viral hepatitis update: Progress and perspectives.World journal of gastroenterology · 2021Review
- Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hepatitis D (CHD) is the most severe form of viral hepatitis, with rapid progression of liver-related diseases and high rates of development of hepatocellular carcinoma. The causative agent, hepatitis D virus (HDV), contains a small (approximately 1.7 kb) highly self-pairing single-strand circular RNA genome that assembles with the HDV antigen to form a ribonucleoprotein (RNP) complex. HDV depends on hepatitis B virus (HBV) envelope proteins for envelopment and de novo hepatocyte entry; however, its intracellular RNA replication is autonomous. In addition, HDV can amplify HBV independently through cell division. Cellular innate immune responses, mainly interferon (IFN) response, are crucial for controlling invading viruses, while viruses counteract these responses to favor their propagation. In contrast to HBV, HDV activates profound IFN response through the melanoma differentiation antigen 5 (MDA5) pathway. This cellular response efficiently suppresses cell-division-mediated HDV spread and, to some extent, early stages of HDV de novo infection, but only marginally impairs RNA replication in resting hepatocytes. In this review, we summarize the current knowledge on HDV structure, replication, and persistence and subsequently focus on the interplay between HDV and IFN response, including IFN activation, sensing, antiviral effects, and viral countermeasures. Finally, we discuss crosstalk with HBV.
Indexed as
Identifiers
What Socratic 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 Socratic graph.