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Persistence of cccDNA during the natural history of chronic hepatitis B and decline during adefovir dipivoxil therapy.
cccDNA persists throughout the natural history of chronic hepatitis B, even in patients with serologic evidence of viral clearance, and long-term ADV therapy significantly decreased cccDNA levels by a primarily noncytolytic mechanism. Expand
Resistance to adefovir dipivoxil therapy associated with the selection of a novel mutation in the HBV polymerase.
The development of this novel mutation in the HBV polymerase confers resistance to adefovir dipivoxil, and the patient responded to subsequent lamivudine therapy, achieving normalization of alanine aminotransferase and a significant decrease in serum HBV DNA. Expand
Intracellular Metabolism and In Vitro Activity of Tenofovir against Hepatitis B Virus
- W. Delaney, A. Ray, +4 authors Michael D. Miller
- Biology, Medicine
- Antimicrobial Agents and Chemotherapy
- 1 July 2006
It is shown that the major adefovir resistance mutation, rtN236T, confers three- to fourfold-reduced susceptibility to tenofovir in cell culture; the clinical significance of this susceptibility shift has not yet been determined. Expand
In Vitro Susceptibility of Adefovir-Associated Hepatitis B Virus Polymerase Mutations to other Antiviral Agents
The results and preliminary clinical data suggest that patients with rtN236T or rtA181V remain susceptible to tenofovir, entecavir and lamivudine, and further clinical data are necessary to precisely define in vitro cutoffs indicative of clinically-relevant resistance, particularly for drugs in development. Expand
Cross-Resistance Testing of Next-Generation Nucleoside and Nucleotide Analogues against Lamivudine-Resistant HBV
- H. Yang, X. Qi, Alex Sabogal, Michael I. Miller, S. Xiong, W. Delaney
- Antiviral therapy
- 1 July 2005
These studies indicate that lamivudine-resistant HBV remain sensitive to acyclic phosphonate nucleotides, have reduced susceptibility to entecavir, and have high-level cross-resistance to all L-nucleosides tested including emtricitabine, telbivUDine, clevudine, and torcitabine. Expand
Cell-Free Hepatitis B Virus Capsid Assembly Dependent on the Core Protein C-Terminal Domain and Regulated by Phosphorylation
A mammalian cell-free system in which HBc is expressed at physiological (low) concentrations and assembles into capsids under near-physiological conditions, which will facilitate detailed studies on capsid assembly and RNA encapsidation under physiological conditions and identification of antiviral agents that target HBc. Expand
Hepatitis B virus genotypes and virologic response in 694 patients in phase III studies of adefovir dipivoxil
HBV genotypes were distributed asymmetrically with respect to race, geography, and HBeAg status, and forty-eight weeks of adefovir dipivoxil therapy resulted in significant decreases in serum HBV-DNA levels in patients regardless of HBV genotype, HBe Ag status, or race. Expand
Hepatitis B virus replication in human HepG2 cells mediated by hepatitis B virus recombinant baculovirus
It is concluded that infection of HepG2 cells by HBV recombinant baculovirus represents a simple to use and highly flexible system for studying the effects of antivirals and/or cytokines on HBV production and for understanding HBV replication and pathogenesis at the molecular level. Expand
In vitro antiviral susceptibility of full-length clinical hepatitis B virus isolates cloned with a novel expression vector.
The development of a new plasmid vector that facilitates the cloning and expression of full-length HBV genomes amplified from the sera of chronic hepatitis B patients and will be useful in future studies including resistance surveillance, cross-resistance analyses, and novel drug-discovery. Expand
The Hepatitis B Virus Polymerase Mutation rtV173L Is Selected during Lamivudine Therapy and Enhances Viral Replication In Vitro
The functional characterization of a third polymerase mutation (rtV173L) associated with resistance to lamivudine and famciclovir is reported, suggesting that rtV 173L is a compensatory mutation that is selected in lamivUDine-resistant patients due to an enhanced replication phenotype. Expand