ArticleNature communications2017
Hepatitis B virus persistence in mice reveals IL-21 and IL-33 as regulators of viral clearance.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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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.
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Who cites it
34 citing papers in PubMed, 50 citations in OpenAlex.
- Antiviral efficacy of LNP-delivered IFN-α14-ApoAI mRNA for chronic hepatitis B.Journal of virus eradication · 2026Article
- Hepatitis B virus promotes liver cancer by modulating the immune response to environmental carcinogens.Nature communications · 2025Article
- Hepatitis B virus surface antigen drives T cell immunity through non-canonical antigen presentation in mice.Nature communications · 2025Article
- Potential role of liver-resident CD3JHEP reports : innovation in hepatology · 2025Article
- Homeobox protein MSX-1 restricts hepatitis B virus by promoting ubiquitin-independent proteasomal degradation of HBx protein.PLoS pathogens · 2025Article
- Transfection of unmodified oligodeoxynucleotide with polyethylenimine reduces the level of hepatitis B surface antigen.Frontiers in microbiology · 2025Article
- Identification and characterization of host factor VCPIP1 as a multi-functional positive regulator of hepatitis B virus.Journal of virology · 2024Article
- Liver mechanosignaling as a natural anti-hepatitis B virus mechanism.Nature communications · 2024Article
- Intrahepatic homeobox protein MSX-1 is a novel host restriction factor of hepatitis B virus.Journal of virology · 2024Article
- The Role of Interleukins in HBV Infection: A Narrative Review.Journal of personalized medicine · 2023Review
- Host and HBV Interactions and Their Potential Impact on Clinical Outcomes.Pathogens (Basel, Switzerland) · 2023Review
- Abnormally primed CD8 T cells: The Achilles' heel of CHB.Frontiers in immunology · 2023Review
- Establishment and characterization of a new cell culture system for hepatitis B virus replication and infection.Virologica Sinica · 2022Article
- Monocytic MDSCs homing to thymus contribute to age-related CD8+ T cell tolerance of HBV.The Journal of experimental medicine · 2022Article
- Innate and adaptive immune escape mechanisms of hepatitis B virus.World journal of gastroenterology · 2022Review
- High mobility group AT-hook 1 (HMGA1) is an important positive regulator of hepatitis B virus (HBV) that is reciprocally upregulated by HBV X protein.Nucleic acids research · 2022Article
- Transient upregulation of EGR1 signaling enhances kidney repair by activating SOX9Theranostics · 2022Article
- Hepatitis B Virus-Specific Cellular Immunity Contributes to the Outcome of Occult Hepatitis B Virus Infection.Frontiers in microbiology · 2022Article
- IFNα subtype-specific susceptibility of HBV in the course of chronic infection.Frontiers in immunology · 2022Article
- Hepatitis B virus middle surface antigen loss promotes clinical variant persistence in mouse models.Virulence · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) generally causes self-limiting infection in immunocompetent adults, but establishes chronic infection in some adults and in most maternally infected infants. Factors determining clearance versus persistence are not fully understood. Hydrodynamic injection (HDI) of HBV replicon plasmid via tail vein generally results in quick clearance in immunocompetent adult mice. Here, we report the identification of strain-specific persistence of HBV in mice: one genotype B strain, designated BPS, persisted up to 33 weeks in ~50% of HDI mice. BPS persistence requires viral replication and multiple viral features. Compared to quickly cleared strains, BPS fails to induce robust post-exposure serum IL-21/IL-33 responses. Injection of IL-21-expressing or IL-33-expressing plasmids facilitates clearance of pre-established BPS persistence and protects cured mice from BPS re-challenge. IL-21 and IL-33 also induce clearance of pre-established HBV persistence in another mouse model. These data reveal IL-21 and IL-33 as potent regulators of HBV clearance and valid drug candidates.
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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.