Genetic susceptibility of serum HBeAg seroconversion in HBeAg-positive patients with chronic hepatitis B
- Author:
WU Yue
;
ZHANG Zhigang
;
GU Ziyang
- Publication Type:Journal Article
- Keywords:
Chronic hepatitis B;
hepatitis B e antigens;
seroconversion;
single nucleotide polymorphism
- From:
China Tropical Medicine
2025;25(3):264-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To screen genetic susceptibility markers related to serum HBeAg seroconversion by analyzing the association between host genetic susceptibility markers and seroconversion in HBeAg-positive patients with chronic hepatitis B (CHB), thereby providing potential molecular markers for clinical outcomes and prognosis evaluation in HBeAg-positive patients with CHB. Methods HBeAg-positive patients with CHB were recruited from the outpatient department of the Infectious Department, Second Affiliated Hospital of Air Force Military Medical University to establish a follow-up cohort. Based on whether HBeAg seroconversion occurred during follow-up, the subjects were divided into a case group (serum HBeAg with seroconversion) and a control group (serum HBeAg without seroconversion). MassARRAY SNP genotyping technique was used to detect SNPs of human genome DNA extracted from whole blood of the study subjects. Results Through association analysis between genetic susceptibility marker SNPs and seroconversion of serum HBeAg, it was found that: At the rs101206 8 locus, under the overdominant model, patients carrying the heterozygous GT genotype had a higher likelihood of serum HBeAg seroconversion (OR=1.73, 95%CI: 1.15-2.59, P=0.008); at the rs352140 locus, under the recessive model, patients carrying the TT genotype had a higher likelihood of serum HBeAg seroconversion (OR=1.77, 95%CI: 1.06-2.94, P=0.029); the rs1946518 locus, under the overdominant model, patients carrying the heterozygous GT genotype had a higher likelihood of serum HBeAg seroconversion (OR=1.73, 95%CI: 1.14-2.61, P=0.009); at the rs2306494 locus, under the dominant model, carrying the A allele (GA+AA) was identified as a negative factor for serum HBeAg seroconversion (OR=0.65, 95%CI: 0.42-0.99, P=0.043); at the rs20541 locus, under the recessive model, carrying the AA genotype was identified as a negative factor for serum HBeAg seroconversion (OR=0.31, 95%CI: 0.10-0.92, P=0.019); at the rs1057035 locus, under the dominant model, patients carrying the C allele (CT+CC) had a higher likelihood of serum HBeAg seroconversion (OR=1.78, 95%CI: 1.05-3.03, P=0.034). Therefore, the GT genotype at rs1012068 of DEPDC5 gene, TT genotype at rs352140 of TLR9 gene, GT genotype at rs1946518 of IL18 gene, and GG genotype at rs2306494 of TERF1 gene were conducive to seroconversion of serum HBeAg. The AA genotype at rs20541 of IL-13 gene and the TT genotype at rs1057035 of DICER1 gene were not conducive to seroconversion of serum HBeAg. Conclusion The genetic susceptibility markers (single nucleotide polymorphism loci) of host genetic genes in HBeAg-positive patients with CHB are associated with seroconversion of serum HBeAg, and the mechanisms by which these SNPs participate in serum HBeAg seroconversion require further investigation.
- Full text:2025111715105250662.Genetic susceptibility of serum HBeAg seroconversion in HBeAg-positive patients with chronic hepatitis B.pdf
