HBV mutation literature information.


  Changes in viral loads of lamivudine-resistant mutants during entecavir therapy.
 PMID: 17573951       2008       Hepatology research
Abstract: Load changes in rtM204I and rtM204V with G1896A tended to be greater than those without.
Abstract: Moreover, G1896A was replaced by wild-type virus in two patients at 52 weeks.


  Maternal chronic hepatitis B virus is implicated with low neonatal paraoxonase/arylesterase activities.
 PMID: 18035058       2008       Clinical biochemistry
Abstract: RESULTS: Serological HBV tests and HBV DNA showed chronic HBV (precore mutant G1896A) in the diseased mothers whereas anti-HBc and anti-HBe were detected in their neonates.


  Maternal chronic hepatitis B virus does not affect neonatal biotinidase activity.
 PMID: 18241289       2008       Acta paediatrica (Oslo, Norway
Abstract: RESULTS: Serological HBV tests and HBV DNA showed chronic HBV (precore mutant G1896A) in group A, whereas anti-HBc and anti-HBe were detected in their neonates.


  Effect of basal core promoter and pre-core mutations on hepatitis B virus replication.
 PMID: 18343830       2008       The Journal of general virology
Abstract: HBeAg was undetectable in all cultures transfected with constructs bearing the G1896A stop-codon mutation, as expected.
Abstract: Substitutions A1762T/G1764A and T1753C, C1766T and T1768A in the BCP region, and G1896A and G1899A in the pre-C region, were examined either alone or in combination, using a common genetic background.
Abstract: The double BCP mutation (A1762T/G1764A) and the pre-C mutations (


  Detection of HBV core promoter and precore mutations helps distinguish flares of chronic hepatitis from acute hepatitis B.
 PMID: 18410611       2008       Journal of gastroenterology and hepatology
Abstract: RESULTS: Mutations in the core promoter (A1762T/G1764A) and precore region (G1896A) were more frequent in patients with acute exacerbation of chronic hepatitis than acute hepatitis (81% vs 19%; P < 0.0001 and 58% vs 6%; P < 0.0001, respectively).


  Analysis of the entire nucleotide sequence of hepatitis B causing consecutive cases of fatal fulminant hepatitis in Miyagi Prefecture Japan.
 PMID: 18428142       2008       Journal of medical virology
Abstract: As for the nucleotides sequences of them, previously reported mutations of G1896A, A1762T, and G1764A were present.


  Application of a novel, rapid, and sensitive oligonucleotide ligation assay for detection of cancer-predicting mutations in the precore and basal core promoter of hepatitis B virus.
 PMID: 18508941       2008       Journal of clinical microbiology
Abstract: Double mutations in the basal core promoter (BCP) (A1762T and G1764A) and precore (pre-C) (G1896A) regions of the virus are associated with progression to HCC.


  [A five-year analysis of HBV mutations in a multidrug-resistant patient with chronic hepatitis B].
 PMID: 18647526       2008       Zhonghua gan zang bing za zhi
Abstract: RESULTS: Several mutations were identified in succession, including LAM-resistant mutations M204I/V and L180M+M204V, ETV-resistant mutation S202G, and HBeAg nonsense mutation G1896A.


  Molecular characterization of hepatitis B virus (HBV) isolates, including identification of a novel recombinant, in patients with acute HBV infection attending an Irish hospital.
 PMID: 18649329       2008       Journal of medical virology
Abstract: One isolate (Irish-13), collected from a patient with acute asymptomatic infection, had a G1896A mutation and a 243 bp deletion of the polymerase gene.
Abstract: Only four isolates from patients with severe HBV infection harbored the G1896A stop codon mutation.


  Associations between hepatitis B virus genotype and mutants and the risk of hepatocellular carcinoma.
 PMID: 18695135       2008       Journal of the National Cancer Institute
Abstract: Among participants with a baseline HBV DNA level of at least 10(4) copies/mL, HCC incidence per 100 000 person-years was higher for those with the precore G1896 (wild-type) variant than for those with the G1896A variant (955.5 [95% CI = 749.0 to 1201.4] vs 269.4 [95% CI = 172.6 to 400.9]) and for those with the BCP A1762T/G1764A double mutant than for those with BCP A1762/G1764 (wild-type) variant (1149.2 [95% CI = 872.6 to 1485.6] vs 358.7 [95% CI = 255.1 to 490.4]).
Abstract: Participants who had a baseline serum HBV DNA level greater than 10(4) copies/mL (n = 1526) were tested for the precore G1896A and



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