The associations between polymorphisms of APOBEC3G and different outcomes of persistent HBV infection.
- Author:
Di TIAN
1
;
Zheng ZENG
;
Guo-bao TIAN
;
Jian-jun CUI
Author Information
- Publication Type:Journal Article
- MeSH: APOBEC-3G Deaminase; Alleles; Asian Continental Ancestry Group; genetics; Cytidine Deaminase; genetics; Female; Gene Frequency; Genotype; Hepatitis B virus; Hepatitis B, Chronic; diagnosis; ethnology; genetics; Humans; Liver Cirrhosis; diagnosis; virology; Male; Middle Aged; Polymorphism, Single Nucleotide; Prognosis; Viral Load
- From: Chinese Journal of Hepatology 2008;16(7):481-486
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the associations between polymorphisms of apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G) and different outcomes of HBV infection in the Chinese Han population.
METHODSSix hundred thirty-five chronic hepatitis B patients were divided into 3 groups: 202, 217 and 216 patients were HBV cleared, chronic hepatitis B, and with liver cirrhosis, respectively. Five tagSNPs (rs8177832, rs17000736, rs17496046, rs9622924 and rs2899313) were genotyped by pyrosequencing. HBV viral loads were determined by real-time PCR method. Chi square was used for statistics.
RESULTSThe majority of rs8177832 allele was A/A and the frequencies of rs8177832 allele among these groups were not significantly different (P more than 0.05). HBV viral loads were higher in chronic hepatitis B patients with G allele than in chronic hepatitis B patients with A allele (P less than 0.05). The rs17000736 and rs9622924 alleles were found only in G/G and C/C genotypes. There were also no significant differences in the other four SNPs alleles (rs17000736, rs17496046, rs9622924 and rs2899313) in these groups (P more than 0.05).
CONCLUSIONSrs8177832, rs17000736, rs17496046, rs17000736 and rs2899313 of the APOBEC3G gene might not be associated with HBV persistent infection in patients in this study. However, the rs8177832 polymorphism may be involved in inhibiting HBV replication.