Abstract: Most OBI strains were wild-type HBV, but some substitutions V168A, S174 N, V177A, Q129R/L/H, G145A/R in S region of genotype B (OBIB) and T47K/V/A, P49H/L, Q101R/H/K, S174 N, L175S, V177A, T118 M/R/K, G145R/A/K/E, R160K/N in S region of genotype C (OBIC) strains were identified in high frequency.
D
Nucleotide Substitutions in Hepatitis B Viruses Derived from Chronic HBV Patients.
PMID: 31308922
2019
Mediterranean journal of hematology and infectious diseases
Abstract: Conclusions: Our results showed common mutations within HBsAg, occurring in immune epitopes, a high rate of G1896A mutations in the PC region, and a negative correlation between the emergence of A1762T/G1764A mutation and the G1764T/C1766G mutant in the BCP region.
Abstract: None of the strains with A1762T/G1764A mutation carried the G1764T/C1766G mutant.
Abstract: The PC and BCP mutations were G1896A (61.0%), PMID: 31324819
2019
Scientific reports
Abstract: Furthermore, we identified novel variants that either independently or in combination with precore mutation G1896A were associated with the transition from HBeAg positive to the negative phase of infection.
Abstract: Patients with viral variants C1817T and A1838G had viral loads nearly three orders of magnitude lower than patients without those variants.
Figure: (b) Patients with high C1817T and A1838G variant frequency (based on 10% cutoff, see methods) had significantly lower HBV DNA levels.
Figure: Black box highlights HBeAg negative patients without detectable viral G1896A variant.
Figure: Columns (patients, N = 1102) are ordere
Association Between HBx Variations and Development of Severe Liver Disease Among Indonesian Patients.
PMID: 31341154
2019
The Kobe journal of medical sciences
Abstract: However, the roles of two novel X gene mutations (A12S/T and L16F/P) on hepatocarcinogenesis are unclear relative to wild-type X gene.
Abstract: In addition, the double mutation K130M/V131I and the triple mutation N88V/K130M/V131I were associated with a 2.5 times higher risk of advanced liver disease.
Locus 5p13.1 may be associated with the selection of cancer-related HBV core promoter mutations.
PMID: 31341412
2019
International journal of medical sciences
Abstract: Background: The basal core promoter (BCP) double mutations (A1762T and G1764A) of hepatitis B virus (HBV) have been reported to be an aetiological factor of hepatocellular carcinoma (HCC).
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 assoc
Next generation sequencing identifies baseline viral mutants associated with treatment response to pegylated interferon in HBeAg-positive chronic hepatitis B.
Abstract: Based on NGS, the prevalence of T1753V (T1753C/A/G) and A1762T/G1764A variants were significantly lower in responders compared to non-responders (8.3% vs.
Abstract: No significant difference between groups was found regarding C1653T and G1896A mutants.
Abstract: The absence of T1753V and A1762T/G1764A mutations were factors associated with CR (OR 11.65, 95%CI 1.36-100.16, P = 0.025, and OR 4.36, 95%CI 1.08-17.63, P = 0.039, respectively).
Abstract: The existence of pre-treatment T1753V, A1762T/G1764A mutations and thei
Investigation of hepatitis B virus (HBV) rtS78T/sC69* mutation in a large cohort of chronic HBV-infected patients with nucleoside/nucleotide analogue treatment.
Abstract: All mutations simultaneously created a stop codon at sC69 (sC69*).
Abstract: Artificial elimination of the rtS78T mutation had a limited effect on the drug susceptibilities.
Abstract: The HBV DNA and RNA levels of the rtS78T/sC69* mutant w
Abstract: The data obtained in the present study suggested that the emergence of the rtS78T/sC69* mutation was not closely related to entecavir/tenofovir treatment and itself appeared insufficient to confer drug resistance unless it coexisted with signature drug-resistance mutations.
rt269I Type of Hepatitis B Virus (HBV) Leads to HBV e Antigen Negative Infections and Liver Disease Progression via Mitochondrial Stress Mediated Type I Interferon Production in Chronic Patients With Genotype C Infections.
Abstract: Our epidemiological study showed HBeAg negative infections of rt269I infections were attributed to a higher frequency of preC mutations at 1896 (G to A).
Result: In addition, the rate of G1986A preC mutation was significant higher in patients with rt269I (49.61%) than those with rt269L (28.
Discussion: Second, our further epidemiologic data showed that HBeAg seronegative status observed in patients with rt269I was due to a higher frequency of preC mutations (G to A at 1896) induced via IFN-I mediated APOBEC3G (Table 2 and Figure 2).
High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank.
Introduction: In addition, double mutation in the basal core promoter (A1762T/G1764A) of HBV genotype C was commonly found as an independent risk factor for the development of HCC.
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 combination mutation involving the double mutation at A1762T/
The modulation of HBsAg level by sI126T is affected by additional amino acid substitutions in the S region of HBV.
PMID: 31442597
2019
Infection, genetics and evolution
Abstract: Among different substitution types at sI126, the sI126T (N = 28) was found to be associated with significantly lower serum HBsAg level.
Abstract: Clone sequencing revealed that sI126T-harboring SHBs sequences had varied genetic backbones with zero to nine additional AA substitutions.
Abstract: Our findings suggest that the modulation of HBsAg level by sI126T is affected by additional AA substitution(s) in the S region of HBV.
Abstract: Thus, we constructed 24 HBsAg expression plasmids harboring s
HBV mutation literature information.
PMID: 
2019
BMC infectious diseases
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