ArticleJournal of virology2002
Replication advantage and host factor-independent phenotypes attributable to a common naturally occurring capsid mutation (I97L) in human hepatitis B virus.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Review
- Persistence of Hepatitis B Virus DNA and the Tempos between Virion Secretion and Genome Maturation in a Mouse Model.Journal of virology · 2019Article
- Naturally occurring core protein mutations compensate for the reduced replication fitness of a lamivudine-resistant HBV isolate.Antiviral research · 2019Article
- HBV maintains electrostatic homeostasis by modulating negative charges from phosphoserine and encapsidated nucleic acids.Scientific reports · 2016Article
- MicroRNA miR-204 and miR-1236 inhibit hepatitis B virus replication via two different mechanisms.Scientific reports · 2016Article
- Impact of the rtI187V polymerase substitution of hepatitis B virus on viral replication and antiviral drug susceptibility.The Journal of general virology · 2014Article
- Hepatitis B virus core protein with hot-spot mutations inhibit MxA gene transcription but has no effect on inhibition of virus replication by interferon α.Virology journal · 2010Article
- A mutant hepatitis B virus core protein mimics inhibitors of icosahedral capsid self-assembly.Biochemistry · 2009Article
- In vitro drug susceptibility analysis of hepatitis B virus clinical quasispecies populations.Journal of clinical microbiology · 2007Article
- Regulation of hepatitis B virus replication by the phosphatidylinositol 3-kinase-akt signal transduction pathway.Journal of virology · 2007Article
- The L80I substitution in the reverse transcriptase domain of the hepatitis B virus polymerase is associated with lamivudine resistance and enhanced viral replication in vitro.Antimicrobial agents and chemotherapy · 2007Article
- Reduced secretion of virions and hepatitis B virus (HBV) surface antigen of a naturally occurring HBV variant correlates with the accumulation of the small S envelope protein in the endoplasmic reticulum and Golgi apparatus.Journal of virology · 2005Article
- Hepatocyte-like cells transdifferentiated from a pancreatic origin can support replication of hepatitis B virus.Journal of virology · 2005Article
- Exposure of RNA templates and encapsidation of spliced viral RNA are influenced by the arginine-rich domain of human hepatitis B virus core antigen (HBcAg 165-173).Journal of virology · 2005Article
- Nucleolar localization of human hepatitis B virus capsid protein.Journal of virology · 2004Article
- Hepatitis B virus capsid assembly is enhanced by naturally occurring mutation F97L.Journal of virology · 2004Article
- The 113th and 117th charged amino acids in the 5th alpha-helix of the HBV core protein are necessary for pgRNA encapsidation.Virus genes · 2003Article
- Stability and morphology comparisons of self-assembled virus-like particles from wild-type and mutant human hepatitis B virus capsid proteins.Journal of virology · 2003Article
- Coexistence of two distinct secretion mutations (P5T and I97L) in hepatitis B virus core produces a wild-type pattern of secretion.Journal of virology · 2003Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations of human hepatitis B virus (HBV) occur frequently within the capsid (core) protein in natural infections. The most frequent mutation of the core protein in HBV from Southeast Asia occurs at amino acid 97, changing an isoleucine (I) to a leucine (L). In our systematic study of virus-host interactions, we have examined the replication efficiency of a site-directed mutant, I97L, and its parental wild-type HBV in several different hepatoma cell lines. Interestingly, we found that this capsid variant replicated in human Huh7 hepatoma cells approximately 4.8-fold better than its parental wild-type HBV. A similar phenomenon was observed in another hepatoma cell line, J3. In addition, the level of encapsidated RNA pregenome in mutant I97L was about 5.7-fold higher than that of the wild-type HBV in Huh7 cells. Unlike Huh7 cells, no significant difference in viral DNA replication between the same I97L mutant and its parental wild-type HBV was observed in HepG2, a human hepatoblastoma cell line. This finding of a profound replication advantage for mutant I97L in Huh7 and J3 cells but not in HepG2 cells may have important implications for the emergence of this mutant in chronic HBV carriers. We speculate here that the mutation confers a host factor-independent growth advantage for the survival of HBV variants in gradually dedifferentiating hepatocytes and thus helps prolong viral persistence.
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