Hepatitis B virus precore/core region mutations and genotypes among hepatitis B virus chronic carriers in South-Eastern, Nigeria.
PMID: 33708042
2021
International journal of health sciences
Discussion: Furthermore, the core gene mutations previously reported to be associated with liver disease progression in chronic patients and particularly in HCC patients such as C1913A/G, C1914G, and G1915T were not identified in any of the sequences from this study.
Pre-S/Surface and Core Promoter/Precore Mutations in Chronic Hepatitis B Patients with Severe Acute Exacerbation.
PMID: 30835025
2019
Digestive diseases and sciences
Abstract: Multivariate analysis showed that the independent factors for SAE were V14G/A and L21S in surface genes, codons 109-119 deletions in pre-S1 genes, M1V/T/I in pre-S2 genes, and C1766T/T1768A and C1913A/G mutations in BCP/PC genes.
Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases.
PMID: 29322851
2018
Scandinavian journal of gastroenterology
Abstract: CONCLUSION: Occurrence of A1846T and C1913A is positively associated with clinical presentations of severe liver disease.
Abstract: In vitro experiment revealed that A1846T mutant resulted in 3.20-fold and 1.85-fold increase of replication capacity and promoter activity, respectively compared with wild type counterpart (p < .001), while C1913A led to a significant decrease of core protein e
Abstract: This study aimed to observe the clinical and virological implications of the A1846T and C1913A/G mutations of HBV genome in the development and treatment outcome of severe liver diseases, which has not been previously determined.
Association of characteristics of HBV quasispecies with hepatitis B surface antigen seroconversion after pegylated interferon-alpha-2a treatment in child patients.
Abstract: The baseline mutations A1762T/G1764A, C1913A, and T2003A/G or C2004T were correlated with non-response to therapy (P=0.025, P=0.036, P=0.032, respectively).
Complete genome sequencing and clinical analysis of intrahepatic hepatitis B virus cccDNA from HCC.
Abstract: Finally, significantly higher levels of preoperative alpha-fetoprotein were observed in patients harboring the G1078T, C1653T, G1727A, C1913A, T1978C, or C3116T mutations at the cccDNA level.
New point mutations in surface and core genes of hepatitis B virus associated with acute on chronic liver failure identified by complete genomic sequencing.
Result: It was found that the old age, genotype B, T216C, G1896A, C1913A/G and A2159G/C mutations were risk factors independently associated with ACLF, as compared with non-ACLF (P < 0.05 or P < 0.01).
Discussion: Multivariate regression analysis showed that T216C, G1896A, C1913A/G and A2159G/C mutations were independent risk factors for ACLF cases.
Discussion: Of these seven mutations, A1846T/G, G1896A and C1913A/G were s
Hepatitis B virus genotype B and mutations in basal core promoter and pre-core/core genes associated with acute-on-chronic liver failure: a multicenter cross-sectional study in China.
Abstract: The A1762T/G1764A, A1846T and G1896A mutations were significantly more common in HB-ACLF patients infected with either genotype B or C as compared with CHB-M, whereas the C1913A/G and A2159G mutations were more associated with HB-ACLF in genotype C patients.
Clinical and virological implications of A1846T and C1913A/G mutations of hepatitis B virus genome in severe liver diseases.
Figure: (B) Proposed secondary structure of the HBV epsilon signal with A1846T and C1913A/G mutations.
Figure: C1913A/G comprised 44.8%, and 50% of ACLF-CHB and ACLF-LC patients.
Discussion: In conclusion, HBV precore mutation of A1846T and the fifth amino acid substitution in the core protein due to C1913A/G were found more frequently in ACLF patients than in their respective CHB or LC patients.
Human interleukin-10 genotypes are associated with different precore/core gene mutation patterns in children with chronic hepatitis B virus infection.
Abstract: RESULTS: HBV precore/core gene mutation increased significantly more in the inflammatory phase than in the tolerance phase (G1896A, 76.2% versus 4.8%; C1913A, 33.3% versus 0%; C2189A, 28.6% versus 4.8%; G2304A, 52.4% versus 14.3%) in study group (n = 21) but not the control group (n = 9).
HBV mutation literature information.
PMID: 
2021
BMC infectious diseases
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