|
Basic Characteristics of Mutations
|
|
Mutation Site
|
G1899A |
|
Mutation Site Sentence
|
T1753V, C1653T, and G1899A were infrequent in the mother-child pairs. |
|
Mutation Level
|
Nucleotide level |
|
Mutation Type
|
Nonsynonymous substitution |
|
Gene/Protein/Region
|
|
|
Standardized Encoding Gene
|
|
|
Genotype/Subtype
|
B;C |
|
Viral Reference
|
-
|
|
Functional Impact and Mechanisms
|
|
Disease
|
Hepatitis B Virus Infection
Carcinoma, Hepatocellular
|
|
Immune
|
- |
|
Target Gene
|
-
|
|
Clinical and Epidemiological Correlations
|
|
Clinical Information
|
Y |
|
Treatment
|
- |
|
Location
|
China |
|
Literature Information
|
|
PMID
|
24973814
|
|
Title
|
Mother-to-child transmission of hepatitis B virus: evolution of hepatocellular carcinoma-related viral mutations in the post-immunization era
|
|
Author
|
Li Z,Xie Z,Ni H,Zhang Q,Lu W,Yin J,Liu W,Ding Y,Zhao Y,Zhu Y,Pu R,Zhang H,Dong H,Fu Y,Sun Q,Xu G,Cao G
|
|
Journal
|
Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
|
|
Journal Info
|
2014 Sep;61(1):47-54
|
|
Abstract
|
BACKGROUND: Perinatal infection and immunoprophylaxis failure of hepatitis B virus (HBV) and viral mutations contributes greatly to the development of hepatocellular carcinoma (HCC). However, little is known regarding evolution of the HCC-related mutations at early stage of chronic infection. OBJECTIVE: We aimed to elucidate dynamic changes of the HCC-related mutations from maternal perinatal transmission to chronic infection in childhood. STUDY DESIGN: A total of 876 hepatitis B surface antigen (HBsAg)-positive pregnant women and 95 HBsAg-positive mother-child pairs were included in this study. HBV mutant quasispecies were determined using clone sequencing. Mother-to-child transmission was identified by genotyping and phylogenestic analysis. RESULTS: Univariate regression analysis indicated that maternal HBeAg positivity, viral load >/=10(6)copies/mL, genotype B2, and male fetus significantly increased the risk of HBV trans-placental transmission. The immunoprophylaxis failure was confirmed in 11 (2.48%) 7-month-old infants. The HCC-risk mutations including A1762T/G1764A were present in the mothers' and cord blood but mostly absent in the 7-month-old infants'. In the 56 mother-child pairs with 1-15 year-old children acquired the infection from their mothers, the frequencies of HBV mutations including A1762T/G1764A and G1896A in genotype B2 or C2 increased consecutively with increasing age of children. These mutations including A1762T/G1764A in genotype C2 and G1896A in genotype B2 were more frequent in mothers than in children (P<0.001). T1753V, C1653T, and G1899A were infrequent in the mother-child pairs. CONCLUSION: Maternally transmitted HBV without the HCC-risk mutations has advantage of infecting infants after the immunization. The HCC-related mutations are sequentially generated since chronic infection established in children.
|
|
Sequence Data
|
KF811606-KF812519;KF840099-KF840131;KJ171072-KJ173446
|
|
|