literature

HBV mutation literature information.

Interaction of mutant hepatitis B X protein with p53 tumor suppressor protein affects both transcription and cell survival.

PMID: 21438026 2011 Molecular carcinogenesis

Introduction: One hotspot mutation involves an adenine to thymine transversion at nucleotide 1762, and a guanine to adenine transition at nucleotide 1764 of the viral genome, and both mutations fall within the X gene (<

Method: Site-directed mutagenesis was then performed on pTracer-WtHBx using mutagenic primers and the QuickChange Site-Directed Mutagenesis Kit (Stratagene, La Jolla, CA), ultimately creating pTracer-MutHBx, which harbors the naturally occurring HBx double mutation A1762T/G1764A.

Figure: Only the two amino acid differences resulting from the A1762T/G1764A base mutations which distinguish MutHBx from WtHBx are indicated.

Association between Hepatitis B Virus X Gene Mutations and Clinical Status in Patients with Chronic Hepatitis B Infection.

PMID: 21461076 2011 Gut and liver

Abstract: RESULTS: Each of the mutations G1386M, C1485T, C1653T, T1753V, A1762T, and G1764A was significantly associated with the patient's clinical status.

Abstract: Specific X gene mutations (G1386M, C1653T, and A1762T/G1764A) were more prevalent in patients with liver cirrhosis and HCC than in chronic hepatitis patients (p<0.005 for all).

Abstract: The T1753V (p<0.001) and

Precore and core promoter mutations of the hepatitis B virus gene in chronic genotype C-infected children.

PMID: 21468263 2011 Journal of Korean medical science

Abstract: The precore (G1896A) and core promoter (A1762T, G1764A) mutations of the hepatitis B virus gene are known to be associated with changes in immunologic phase or the progression to complicated liver disease in adults.

Introduction: Precore mutations, such as G1896A (guanine-to-adenine mutation at nucleotide 1,896), and core promoter (CP) mutations, including A1762T (adenine-to-thymine mutation at nucleotide 1,762) and G1764A (guanine-to-adenine mutation at nucleotide 1,764), are known to be associated with HBeAg stat

Impact of hepatitis B virus (HBV) x gene mutations on hepatocellular carcinoma development in chronic HBV infection.

PMID: 21490166 2011 Clinical and vaccine immunology

Abstract: The hepatitis B virus (HBV) PreS mutations C1653T, T1753V, and A1762T/G1764A were reported as a strong risk factor of hepatocellular carcinoma (HCC) in a meta-analysis.

Full genome characterization of hepatitis B virus strains from blood donors in Iran.

PMID: 21503905 2011 Journal of medical virology

Abstract: The double mutations A1762T/G1764A and G1764T/C1766G were found in 20.7% and 24.1% of the strains, respectively.

Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants.

PMID: 21562108 2011 Journal of clinical microbiology

Abstract: Hepatitis B virus (HBV) carrying the A1762T/G1764A double mutation in the basal core promoter (BCP) region is associated with HBe antigen seroconversion and increased risk of liver cirrhosis and hepatocellular carcinoma (HCC).

A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B patients.

PMID: 21569538 2011 Virology journal

Introduction: G1896A variation was mainly present in patients who were HBeAg-negative natives of Asian or Mediterranean basin, whereas A1762T/G1764A dual variations were detected in a similar proportion of HBeAg-negative and HBeAg-positive patients.

Introduction: In addition to genotype B, G1896A variation, not A1762T/G1764A dual variations, is proposed to be another major mechanism to explain spontaneous HBeAg loss in the natural history of chronic HBV infection.

Unsuccessful therapy with adefovir and entecavir-tenofovir in a patient with chronic hepatitis B infection with previous resistance to lamivudine: a fourteen-year evolution of hepatitis B virus mutations.

PMID: 21696601 2011 BMC infectious diseases

Abstract: The precore/core frame A1762T and G1764A double mutation was detected before treatment and remaining in this condition during the entire follow-up.

Conclusion: The HBV genomic characterization at preC-C level showed the presence of A1762T and G1764A double mutation that was early detected when the patient was untreated, remaining in this condition during the entire follow-up.

Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21.

PMID: 21704589 2011 Gastroenterology

Abstract: METHODS: We constructed a series of HBx mutants with changes in the CP region that correspond to A1762T/G1764A (TA), T1753A, T1768A, or a combination of these (combo) and expressed them, along with wild-type HBx under control of its endogenous promoter, in primary human hepatocytes (PHHs) and HepG2 cells.

Introduction: Clinical studies have shown that the common double mutation A1762T/G1764A (TA) in the HBV basal core promoter (CP) region is independently associated with HCC.

Discussion: Our results in He

Differences in HBV Replication, APOBEC3 Family Expression, and Inflammatory Cytokine Levels Between Wild-Type HBV and Pre-core (G1896A) or Basal Core Promoter (A1762T/G1764A) Mutants.

PMID: 21739444 2011 Journal of medical virology

Abstract: In conclusion, CHB patients with genotype B, G1896A, and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C.

Abstract: In genotype B patients, the A1762T/G1764A, A1846T, and G1896A mutations were significantly more prevalent in patients with acute-on-chronic liver failure than CHB (50.7% vs.

Abstract: In multivariate analysis, the risk factors for acute-on-chronic liver failure were genotype B, A1762T/

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