literature

HBV mutation literature information.

Clustering infection of hepatitis B virus genotype B4 among residents in Vietnam, and its genomic characters both intra- and extra-family.

PMID: 28753615 2017 PloS one

Result: There were no C1653T mutations, two (4.5%) T1753V mutations, five (11.4%) double mutations of A1762T/G1764A, and three (6.8%) double mutations of C1766T/T1768A.

Discussion: But looking at the promoter region mutations, G1613A mutation was identified in 10.3% of these 31 strains, C1653T was 0%, T1753V was 3.2%, A1762T/G1764A was 16.1%, and C1766T /T1768A was 3.2%.

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: Among these clones, 13 (9 from HCC patients) harbored additional T1753C mutation (Fig. 1), 2 had additional C1766T mutation.

Result: In this regard 7 of the 12 highest replicating clones harbored either T1753C or C1766T.

Result: Our previous studies found that T1753C and C1766T could enhance the replication promoting effect of A1762T/G1764A hot spot mutations in genotype A.

HBV core promoter mutations and AKT upregulate S-phase kinase-associated protein 2 to promote postoperative hepatocellular carcinoma progression.

PMID: 27779207 2016 Scientific reports

Introduction: In addition to TA, other CP mutations, notably C1653T, T1674C/G, C1766T, T1753V and T1768A, have also been reported to be associated with an increased risk of HCC.

Fatal fulminant hepatitis caused by infection with subgenotype A1 hepatitis B virus with C1766T/T1768A core promoter mutations.

PMID: 27473751 2016 The Journal of general virology

Abstract: The present study demonstrates that the C1766T/T1768A mutations in the BCP region of genotype A HBV enhance viral replication, downregulate HBeAg expression and are responsible for the predominant localization of the core protein in the cytoplasm, which are likely associated with the development of fulminant hepatitis.

Abstract: We recently found four unique mutations [G to A at nucleotide 1742 (G1742A), C1766T, T1768A and T1809C] in the basal core promoter (BCP) region of a genotype A hepatitis B vi

Fatal fulminant hepatitis caused by infection with subgenotype A1 hepatitis B virus with C1766T/T1768A core promoter mutations.

PMID: 27165167 2016 Clinical journal of gastroenterology

Abstract: Here, we present a case of fatal fulminant hepatitis caused by infection with subgenotype A1 hepatitis B virus with C1766T/T1768A double mutations in the core promoter region.

Hepatitis B virus basal core promoter mutations show lower replication fitness associated with cccDNA acetylation status.

PMID: 27132039 2016 Virus research

Abstract: HBV monomers bearing BCP mutations A1762T/G1764A and A1762T/G1764A/C1766T, and precore mutations G1896A, G1899A and G1896A/G1899A, were transfected into HepG2 cells using a plasmid-free approach.

Associations between hepatitis B virus basal core promoter/pre-core region mutations and the risk of acute-on-chronic liver failure: a meta-analysis.

PMID: 26063382 2015 Virology journal

Abstract: Several mutations were significantly correlated with ACLF: T1753V (1.889, 95 % confidence interval (CI) [1.357-2.631]), A1762T (2.696 [2.265-3.207]), G1764A (3.005 [2.077-4.

Conclusion: The HBV BCP/PC mutations T1753V, A1762T, G1764A, C1766T, T1768A, A1846T, G1896A and G1899A, and an HBeAg-negative status correlate with an increased risk of HBV-ACLF.

G1896A Precore Mutation and Association With HBeAg Status, Genotype and Clinical Status in Patients With Chronic Hepatitis B.

PMID: 26587040 2015 Hepatitis monthly

Abstract: The basal core promoter mutations detected were A1762T-G1764A (26.9%), C1653T (8.6%), A1752G (10.8%) and C1766T (2.2%).

Result: Among the basal core promoter mutations, A1762T-G1764A double mutation was present in 26.9%, C1653T in 8.6%, A1752G in1 0.8% and C1766T in 2.2% of all isolates.

Table: C1766T

Virological Characteristics of Acute Hepatitis B in Eastern India: Critical Differences with Chronic Infection.

PMID: 26571502 2015 PloS one

Result: It is noteworthy, that the C69stop codon mutation in the surface gene, the C1766T /T1768A mutation in the basal core promoter and the H94Y mutation in the x gene were found only in chronic patients.

Result: The C1766T/T1768A double mutation was however detectable in only chronic infection (2%).

Discussion: Among them the C69stop codon mutation in the surface gene, the C1766T /T1768A mutation in the basal core promoter and the

Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma.

PMID: 25881591 2015 Chinese medical journal

Introduction: We and others have reported that HBV mutations C1653T, T1753V, A1762T/G1764A, T1674C/G, and C1766T/T1768A in the enhancer II/basal core promoter (EnhII/BCP) region; G1899A, C2002T, A2159G, A2189C, and G2203A/T in the precore/core region; as well as T53C,

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