ArticleJournal of virology2012
Viral-load-dependent effects of liver injury and regeneration on hepatitis B virus replication in mice.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 13 citations in OpenAlex.
- Virus-host interaction mechanisms in interferon therapy for hepatitis B virus infection: recent advances.Frontiers in immunology · 2025Review
- Pathogenicity and virulence of Hepatitis B virus.Virulence · 2022Review
- Interferon and interferon-stimulated genes in HBV treatment.Frontiers in immunology · 2022Review
- Hepatitis B Virus Reactivation in Cancer Patients Undergoing Immune Checkpoint Inhibitors Therapy: A Systematic Review.Journal of Cancer · 2022Review
- Mechanisms of Hepatitis B Virus Persistence.Trends in microbiology · 2018Review
- Emergence of Leptin in Infection and Immunity: Scope and Challenges in Vaccines Formulation.Frontiers in cellular and infection microbiology · 2018Review
- Hepatitis B virus inhibits insulin receptor signaling and impairs liver regeneration via intracellular retention of the insulin receptor.Cellular and molecular life sciences : CMLS · 2016Article
- Technical standards for hepatitis B virus X protein (HBx) research.Hepatology (Baltimore, Md.) · 2015Review
- A MAVS/TICAM-1-independent interferon-inducing pathway contributes to regulation of hepatitis B virus replication in the mouse hydrodynamic injection model.Journal of innate immunity · 2015Article
- Foxa3 induces goblet cell metaplasia and inhibits innate antiviral immunity.American journal of respiratory and critical care medicine · 2014Article
- 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Hepatitis B virus (HBV) is a hepatotropic virus that can cause severe liver diseases. By conducting studies using four different transgenic mouse lines that carry either the wild-type HBV genome or the HBV genome incapable of expressing the X gene, we found that liver injury and regeneration induced by a partial hepatectomy (PHx) could have different effects on HBV replication depending on the mouse lines. Further studies using hydrodynamic injection to introduce different amounts of the HBV genomic DNA into the mouse liver revealed that liver injury and regeneration induced by PHx enhanced HBV replication when viral load was low and suppressed HBV replication when viral load was high. These effects of liver injury and regeneration on HBV were independent of the HBV X protein and apparently due to alpha and beta interferons (IFN-α/β), as the effects could be abolished by the injection of anti-IFN-α/β antibodies. Further analysis indicated that PHx could induce the expression of hepatocyte nuclear factor 3 gamma (HNF3γ) when viral load was low and activate the signal transducer and activator of transcription 3 (Stat3) and suppress the expression of the suppressor of cytokine signaling 3 (SOCS3) irrespective of viral load. As both HNF3γ and Stat3 are required to activate the HBV enhancer I to stimulate HBV gene expression and replication, these results provided an explanation to the viral-load-dependent effect of liver injury and regeneration on HBV replication. Our studies thus revealed a novel interaction between HBV and its host and provided important information for understanding HBV replication and pathogenesis during liver injury.
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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.