Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies.
Result: In the level of nucleotide, the double mutations A1762T/G1764A in the BCP region of HBV (nt1742-1849) were frequently observed in HBV/CD sequences (50/179, 27.9%).
Table: A1762T
Discussion: In this study, the A1762T/G1764A double mutations were observed in 27.93% in HBV CD recombinant sequences.
Discussion: Previous studies reported that A1762T/G1764A double mutation in BCP (nt.1742-1849) was the strongest viral factor associated with the development of liver disease.
In silico Analysis of Genetic Diversity of Human Hepatitis B Virus in Southeast Asia, Australia and New Zealand.
Abstract: The three HBV variants identified most frequently were p.V5L, c.1896G>A and double mutation c.1762A>T/c.1764G>A, while genotypes B and C had the widest range of mutation types.
The genetic variability of hepatitis B virus subgenotype F1b precore/core gene is related to the outcome of the acute infection.
Abstract: Mutations T1753C, A1762T, G1764A, C1766T, T1768A G1896A, G2092T and T2107C were associated with acute liver failure and progression to chronic hepatitis.
Case Report: Application of hepatitis B virus (HBV) deep sequencing to distinguish between acute and chronic infection.
Abstract: HCC-associated mutations were detected in 33.7% of the sequences, with significantly higher frequency of C1653T, T1753V and A1762T/G1764A in genotype G than C (P < 0.001).
Result: C1653T, T1753V and A1762T/G1764A were highly frequent in genotype G (95, 95, and 97.5%, respectively), followed by genotype C (12, 18.1, and 46.1%, respectively), while Pre-S deletions prevailed in genotype C (3.3%) (Table 1).
Result: Significant differences in A1762T/G1764A rates were found within genotypes B, C, D, and F, with subgenotypes B
An Association Between Core Mutations in Hepatitis B Virus Genotype F1b and Hepatocellular Carcinoma in Alaskan Native People.
Abstract: In the HCC patients, T1938C and A2051C mutations in the core region had accumulated significantly with A1762T/G1764A mutations in the basal core promoter (BCP) region and G1896A mutation in the precore (PC) region.
Hepatitis B virus in Mar del Plata, Argentina: Genomic characterization and evolutionary analysis of subgenotype F1b.
Abstract: The double substitution G1764A/A1762T at the BCP (reduced HBeAg expression) was found in 20% F1b, 2% A2, 2% D1, and 2% D3 samples.
Naturally Occurring Mutations within HBV Surface Promoter II Sequences Affect Transcription Activity, HBsAg and HBV DNA Levels in HBeAg-Positive Chronic Hepatitis B Patients.
Introduction: For instance, it was found that A1762T/G1764A were novel mutations within CP and could lead to decreased HBeAg expression but enhanced viral replication, which correlated with liver disease severity.
Discussion: Whether single-site mutations may have such a significant effect on activity, we refer to the effects of the A1762T/G1764A mutation in HBV.
HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism.
Discussion: Taken together, these results provide a potential mechanism whereby HBV encoding X_K130M/V131I (BCP_A1762T/G1764A) may contribute to the high rate of HCC observed clinically in patient cohorts containing these mutations.
Discussion: The X_K130M/V131I amino acid changes are encoded by nucleotide changes at BCP_A1762T/G1764A, which also result in a decrease in PC/C mRNA and subsequent HBeAg expression.
A substitution in the pre-S1 promoter region is associated with the viral regulation of hepatitis B virus.
Introduction: Double mutations, A1762T and G1764A, in the basic core promoter region result in decreased HBeAg expression and enhanced viral genome replication; these mutations are frequently found in HBeAg-negative chronic hepatitis patients.
Discussion: The A1762T and G1764A mutations in the basic core promoter region are associated with an increased risk of HCC in genotype C patients.
HBV mutation literature information.
PMID: 
2020
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