ArticleThe Journal of clinical investigation2001
X-deficient woodchuck hepatitis virus mutants behave like attenuated viruses and induce protective immunity in vivo.
Article in The Journal of clinical investigation, 2001. 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.
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
34 citing papers in PubMed, 62 citations in OpenAlex.
- The Intrinsically Disordered Region of HBx and Virus-Host Interactions: Uncovering New Therapeutic Approaches for HBV and Cancer.International journal of molecular sciences · 2025Review
- Understanding the genetics of viral drug resistance by integrating clinical data and mining of the scientific literature.Scientific reports · 2022Article
- Canonical and Divergent N-Terminal HBx Isoform Proteins Unveiled: Characteristics and Roles during HBV Replication.Biomedicines · 2021Article
- Relevance of reactive oxygen species in liver disease observed in transgenic mice expressing the hepatitis B virus X protein.Laboratory animal research · 2020Review
- A Role for the Host DNA Damage Response in Hepatitis B Virus cccDNA Formation-and Beyond?Viruses · 2017Review
- Virology: The X-Files of hepatitis B.Nature · 2016Article
- Hepatocyte Factor JMJD5 Regulates Hepatitis B Virus Replication through Interaction with HBx.Journal of virology · 2016Article
- Hepatitis B Virus X and Regulation of Viral Gene Expression.Cold Spring Harbor perspectives in medicine · 2016Review
- Hepatitis B virus molecular biology and pathogenesis.Hepatoma research · 2016Article
- The Woodchuck, a Nonprimate Model for Immunopathogenesis and Therapeutic Immunomodulation in Chronic Hepatitis B Virus Infection.Cold Spring Harbor perspectives in medicine · 2015Review
- Molecular biology of hepatitis B virus infection.Virology · 2015Review
- Animal models and the molecular biology of hepadnavirus infection.Cold Spring Harbor perspectives in medicine · 2015Review
- Review
- HBV induced HCC: major risk factors from genetic to molecular level.BioMed research international · 2013Review
- Hepatitis B virus X gene and hepatocarcinogenesis.Journal of gastroenterology · 2011Review
- Hepatitis B and C virus hepatocarcinogenesis: lessons learned and future challenges.Cancer letters · 2011Review
- The C-terminal region of the hepatitis B virus X protein is essential for its stability and function.Virus research · 2011Article
- Inhibition of cellular proteasome activities mediates HBX-independent hepatitis B virus replication in vivo.Journal of virology · 2010Article
- Pathogenesis of hepatitis B virus infection.Pathologie-biologie · 2010Review
- Nuclear HBx binds the HBV minichromosome and modifies the epigenetic regulation of cccDNA function.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The X protein (HBX) of the hepatitis B virus (HBV) has been shown to be important for the establishment of HBV infection in vivo. Our previous studies suggested that interaction of HBX with the proteasome complex may underlie the pleiotropic functions of HBX. In this study, we generated a series of woodchuck hepatitis virus (WHV) X mutants, including mutants of the domain interacting with the proteasome, and studied their infectivity in woodchucks. Many of the mutants were defective in transactivation but none of them were completely replication defective in vitro. In vivo, all the wild-type and some X mutant-transfected animals demonstrated evidence of infection with anti-WHc and/or anti-WHs seroconversion. Most of the wild-type- and X mutant-transfected animals had transient viremia. Some animals were later challenged with infectious WHV. Animals inoculated with X mutants, including those with no serologic evidence of infection, were protected from the challenge, suggesting previous infection with resulting protective immunity. Our study demonstrates that the previously described functional domains of HBX are biologically important and the X-defective mutants, possibly as attenuated viruses, are not completely replication defective in vivo.
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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.