HBV mutation literature information.


  Pro-oncogenic, intra host viral quasispecies in Diffuse large B cell lymphoma patients with occult Hepatitis B Virus infection.
 PMID: 31601912       2019       Scientific reports
Abstract: In tumor compartments per se, several mis-sense mutations were detected, notably the classic T1762A/A1764G mutation in the basal core promoter.
Table: T1762A
Discussion: Most notable of these and found in all seven tumor samples analyzed in our study was the classic double mutation T1762A/A1764G, in the basal core promoter region (BCP) which has been reported in several studies and is known to be an important pro-oncogenic mutation.


  Sequence analysis and functional characterization of full-length hepatitis B virus genomes from Korean cirrhotic patients with or without liver cancer.
 PMID: 28373061       2017       Virus research
Result: The T1762A/A1764G back mutations markedly reduced genome replication for clone 4.2, whereas the A1896G back mutation had limited effect.


  Naturally occurring basal core promoter A1762T/G1764A dual mutations increase the risk of HBV-related hepatocellular carcinoma: a meta-analysis.
 PMID: 26848866       2016       Oncotarget
Discussion: Transfection studies have shown that the T1762A/G1764A dual mutations decrease the level of pre-C mRNA by 50% to 70%, thereby inhibiting HBeAg production.


  Lower mutation frequency of BCP/precore regions in e antigen-negative chronic HBV-infected children instead of adults patients.
 PMID: 25822176       2015       PloS one
Discussion: The other is a two-nucleotide substitution, T1762A and G1764A, and transfection studies have shown that the T1762A and G1764A double mutation decreases the level of pre-C mRNA by 50% to 70%, leading to reduced HBeAg synthesis.


  The Effect of HBV Genotype C on the Development of HCC Differs Between Wild-Type Viruses and Those With BCP Double Mutations (T(1762)A(1764)).
 PMID: 24693312       2014       Hepatitis monthly
Abstract: HBV basal core promoter (BCP) double mutations (T(1762)A(1764)) are very strong confounding factors of genotypes B and C in HCC development.


  [Results of a novel real-time PCR, sequence analysis, Inno-LiPA line probe assays in the detection of hepatitis B virus G1896A precore mutation in French blood donors].
 PMID: 20843617       2011       Pathologie-biologie
Abstract: AIM: To screen hepatitis B virus (HBV) genotypes and associated basal core promoter (BCP; T1762A/A1764) and precore (PC; A1896) mutations among the 100 HBV surface antigen (HBsAg) positive voluntary blood donors in France.


  CTL escape mutations of core protein are more frequent in strains of HBeAg negative patients with low levels of HBV DNA.
 PMID: 19748824       2009       Journal of clinical virology
Abstract: By multivariate analysis, high level (>10(5)copies/mL) of serum HBV DNA was inversely associated with the presence of mutations in CTL epitopes of HBc (OR: 0.11, p=0.015), while it was directly associated with the presence of promoter double T(1762)A(1764) mutations together with G(1757) (OR: 16.87, p=0.004).


  A1762T/G1764A mutations of hepatitis B virus, associated with the increased risk of hepatocellular carcinoma, reduce basal core promoter activities.
 PMID: 18675784       2008       Biochemical and biophysical research communications
Abstract: We also show that T1762A and G1764A double mutations synergize the reduction of the promoter activity.


  Molecular epidemiological study of hepatitis B virus infection in two different ethnic populations from the Solomon Islands.
 PMID: 17245721       2007       Journal of medical virology
Abstract: While the prevalence of the BCP mutation (T(1762)A(1764)) tended to be higher in HBV/C, that of the Pre-C mutation (T(1846)) was significantly higher in HBV/D (P < 0.0001).


  Clinical outcome and virological characteristics of hepatitis B-related acute liver failure in the United States.
 PMID: 15720535       2005       Journal of viral hepatitis
Abstract: Prevalence of HBV genotypes, precore stop (G1896A) and core promoter dual (T1762A, A1764T) variants among patients with HBV-ALF were compared with a cohort of 530 patients with chronic HBV infection.



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