Abstract: Wild-type HBx (WT-HBx) and four HBx mutants (M1, A1762T/G1764A; M2, T1674G+T1753C+A1762T/G1764A; M3, C1653T+T1674G+A1762T/G1764A; and Ct-HBx, carboxylic acid-terminal truncated HBx) were delivered into Sleeping Beauty (SB) mouse models.
Introduction: HBV mutations, including A1762T/G1764A, C1653T, T1753V,
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: Nucleotide mutations, including A1984G, T150AC, A2735C, C2523G, A37G, C2712AT, and C1653T were dramatically different in CD1 and CD2, though these mutations were in the same recombination regions (genotype C or genotype D fragment).
Table: C1653T
Discussion: Other mutations, such as T53C, G1613A, C1653T, T1753C, A2189C, T3098C and PreS deletions were also reported associated with clinical progress.
Discussion: The sa
The genetic polymorphism down-regulating HLA-DRB1 enhancer activity facilitates HBV persistence, evolution and hepatocarcinogenesis in the Chinese Han population.
Abstract: rs3135395-T, rs477515-T and rs2395178-G were inversely associated with the generation of A1762T/G1764A, T1753V and C1653T, the HCC-risk HBV mutations.
Comprehensive Analysis of Clinically Significant Hepatitis B Virus Mutations in Relation to Genotype, Subgenotype and Geographic Region.
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: The frequencies of C1653T, T1753V and A1762T/ PMID: 31324819
2019
Scientific reports
Result: Aside from C1817T and A1838G variants, it is worth mentioning that C1653T, G1896A, and G1899A displayed the next most significant association with viral load in the discovery patient cohort (LRT p = 6 x 10-8, p = 6.7 x 10-8, and p = 2.3 x 10-7, respectively).
Result: Specifically, C1653T alters the binding site of the CAAT enhancer-binding protein of the alpha-box within the HBV enhancer II region, which is known to transcriptionally regulate the pgRNA.
Discussion: C1653T exhibited only marginal signal with viral load.
Discussion: Previous studies described additional variants in the core promoter including
Locus 5p13.1 may be associated with the selection of cancer-related HBV core promoter mutations.
PMID: 31341412
2019
International journal of medical sciences
Introduction: The precore mutation (G1896A), mutations in enhancer II (C1653T) and the BCP (T1753V and the double mutations, A1762T, G1764A), and deletions in the pre-S region have been reported to be associated with the development of HCC.
Next generation sequencing identifies baseline viral mutants associated with treatment response to pegylated interferon in HBeAg-positive chronic hepatitis B.
Abstract: Multiple mutations were confirmed in 24 Cambodian C1 isolates, especially double mutation at A1762T/G1764A in 18 isolates (75.0%), and combination mutation at C1653T and/or T1753V and A1762T/G1764A in 14 isolates (58.3%).
Introduction: Mutations at C1653T and/or T1753V and A1762T/G1764A in Enhancer II/basal core promoter were also reported to be associated with HCC in 1999 compared with other liver disease statuses.
Introduction: The c
Qidong hepatitis B virus infection cohort: a 25-year prospective study in high risk area of primary liver cancer.
Introduction: By using capillary gel electrophoresis, we found that it was the short fragment, rather than larger fragment, contributing to the association of Pre-S deletion with HCC., In addition to the above novel findings, we also verified the association of some known HBV mutations, such as HBV pre-S2 start codon mutation, C1653T and T1753C, with HCC in Qidong.
Introduction: While A1762T/G1764A, C1653T, A799G, A987G, T1055A, pre-S deletion could be detected in the plasma long
HBV mutation literature information.
PMID: 
2022
PloS one
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