Disease relevance of WhBvgp1

• The incomplete DNA strand, however, which is the strand elongated by the virion DNA polymerase reaction, did not contain a detectable amount of polypeptide as did the complete strand [1].
• Three of them had consistently elevated levels of circulating Dane-particle markers, including Dane-particle-associated DNA polymerase activity, hepatitis B core antigen and Dane-particle-associated DNA [2].
• Inhibition of hepatitis B DNA polymerase by intercalating agents [3].
• Patients with chronic hepatitis B with active viral replication had a significantly greater fall in DNA polymerase and hepatitis-Be antigen when treated with interferon and acyclovir together than when treated with either interferon or acyclovir alone [4].
• These particles produced in vitro were also indistinguishable from the naturally occurring hepatitis B virions in containing the virus-associated DNA polymerase and mature HBV genomes [5].

High impact information on WhBvgp1

• Intracellular WHV core particles, containing WHV DNA replication intermediates, RNA/DNA hybrid molecules, and an active endogenous DNA polymerase, appeared 3 days after the start of LPS stimulation [6].
• Serum components inhibit DNA polymerase, thereby obviating direct detection of serum viral DNA sequences by the polymerase chain reaction (PCR) [7].
• We conclude that foscarnet exerts its effect in hepadna virus infection through inhibition of viral DNA polymerase [8].
• Extended lamivudine treatment leads to the development of a specific lamivudine-resistant virus with base-pair substitutions at the YMDD locus of the DNA polymerase [9].
• However, HBV resistance to lamivudine has been reported and shown to have amino acid substitutions in the methionine residue of the conserved tyrosine (Y), methionine (M), aspartate (D), aspartate (D) motif of RNA-dependent DNA polymerase [10].

Chemical compound and disease context of WhBvgp1

• The use of L(-)SddC [beta-L-2',3'-dideoxy-3'-thiacytidine (lamivudine, 3TC)] for the treatment of Herpes B virus (HBV) infection is hindered by the emergence of drug-resistance associated with the L526M, L550V, and L526M/M550V mutations of the viral DNA polymerase (DP) [11].
• Like human hepatitis B virus DNA polymerase, the woodchuck hepatitis virus DNA polymerase was strongly inhibited by phosphonoformic acid but not by phosphonoacetic acid and aphidicolin [12].
• Suramin, a polybasic anion, blocks the activity of the DNA polymerase encoded by the duck hepatitis B virus [13].
• Efficacy of famciclovir treatment in chronic hepatitis B patients with different mutations at position 552 of the DNA polymerase gene [14].
• These mutations in the HBV polymerase gene were located in a similar area to the penciclovir-induced mutations observed in the herpes simplex virus DNA polymerase gene [15].

Biological context of WhBvgp1

• DNA was isolated from the ayw subtype of hepatitis B virus (HBV) that had been incubated in vitro with all four deoxynucleoside triphosphates in order to complete the circular viral genome by means of the endogenous DNA polymerase [16].
• However, the emergence of lamivudine-resistant mutant virus, with amino acid substitution in the YMDD motif of DNA polymerase, has been reported [17].
• However, nucleocapsids were not enveloped or secreted when they were produced by an HBV genome carrying a missense mutation in the DNA polymerase that eliminates all DNA synthesis [18].
• Three WHV variants with mutations in the active site of the DNA polymerase gene are present at this time (W. S. Mason et al., Virology 245:18-32, 1998) [19].
• Transfection results showed that the plasmid-containing mutations of the C gene significantly decreased the DNA polymerase activity in virions [20].

Anatomical context of WhBvgp1

• We detected the supercoiled form of DHBV DNA, DHBV RNA transcripts similar to those in the virus-replicating liver, and DNA polymerase activity and viral DNA in corelike particles in extracts of yolk sac tissue of naturally infected eggs [21].
• Membranous display of pre-S2 on hepatocytes was observed more often in DNA polymerase-positive patients, and their serum pre-S2 levels were significantly higher than those without it [22].
• Transfection of this HBV variant clone into the human hepatoma cell line HepG2 resulted in the appearance of major HBV transcripts, replicative forms of viral DNA evidenced by both molecular hybridization and endogenous DNA polymerase assay, as well as the expression and secretion of HBsAg and HBcAg particles [23].
• This paper describes an assay for hepatitis B DNA polymerase which is based on the use of phosphonoformic acid (PFA), a known inhibitor of the viral enzyme, with particulate fractions prepared from blood plasma or serum [24].
• However, the DNA polymerase activated by calf thymus DNA was inhibited by 0.4 M KCl [25].

Associations of WhBvgp1 with chemical compounds

• We conclude that adenine arabinoside likely exerts its effect in hepadna virus infections predominantly through inhibition of viral DNA polymerase [26].
• In the anti-HBe positive patients, 14 starting therapy and eight untreated, there were no significant changes in the markers of viral replication - although two patients developed DNA polymerase activity on high maintenance doses of prednisolone - but a significant decrease (p less than 0.05) in aspartate transaminase in the treated group [27].
• The interactions of the anti-HBV compounds 2',3'-dideoxy-2',3'-didehydro-beta-L(-)-5-fluorode-oxycytidine and 2'-fluoro-5-methyl-beta-L-arabinofuranosyluracil triphosphate with HBV DP and its L(-)SddC-associated mutants have not been studied [11].
• Oral acyclovir had no detectable effect on DNA-polymerase or HBeAg [28].
• In the last 2.5 years of famciclovir treatment, an increase in serum HBV DNA levels and a reduced sensitivity of the virion-associated DNA polymerase to penciclovir triphosphate were observed [15].

Analytical, diagnostic and therapeutic context of WhBvgp1

• Fractionation of these particles by CsCl density equilibrium gradient centrifugation and assay of the fractions for surface antigen, core antigen, and DNA polymerase activities demonstrate the presence of all three at an approximate density peak of 1.27 [29].
• All the progeny were, on evaluation for congenital infection, found to be duck hepatitis B virus positive by endogenous DNA polymerase reaction and electron microscopy [30].
• Four patients were HBsAg, HBeAg, DNA polymerase, and HBV DNA positive prior to transplantation, and these markers persisted [31].
• An assay for DNA polymerase reaction products using slab gel electrophoresis and autoradiography was compared with the spot hybridization technique for the detection of hepatitis B virus DNA in 317 blood samples [32].
• Biopsies were analyzed for HBcAg, HBsAg, and delta antigen by immunofluorescence; sera were assayed for HBsAg/anti-HBs, HBcAg/anti-HBc, HBeAg/anti-HBe, delta/anti-delta, HBV-specific DNA polymerase activity and the presence of HBV DNA [33].

References