Influence of copy number variations in the FCGR3A and FCGR3B genes on the outcome of hepatitis B virus infection
10.3969/j.issn.1001-5256.2022.06.012
- VernacularTitle:FCGR3A和FCGR3B基因拷贝数变异对HBV感染转归的影响
- Author:
Haotian LI
1
;
Tongtong WANG
1
;
Xutong LI
1
;
Yufeng GAO
1
Author Information
1. Department of Infectious Diseases, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China
- Publication Type:Original Articles_Viral Hepatitis
- Keywords:
Hepatitis B virus;
DNA Copy Number Variations;
Immunoglobulin G
- From:
Journal of Clinical Hepatology
2022;38(6):1275-1279
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the association of copy number variations (CNVs) in the FCGR3A and FCGR3B genes with different outcomes and disease progression after hepatitis B virus (HBV) infection. Methods Peripheral blood samples were collected from 841 patients with chronic HBV infection and 296 patients with self-limited HBV infection, an according to the degree of disease progression, the patients with chronic HBV infection were further divided into chronic hepatitis B (CHB) group, liver cirrhosis (LC) group, and hepatocellular carcinoma (HCC) group. The AccuCopy technique was used for the quantitative analysis of CNVs in the FCGR3A and FCGR3B genes in peripheral blood. The independent samples t -test was used for comparison of continuous data between two groups, and a one-way analysis of variance and the Kruskal-Wallis H test were used for comparison between multiple groups; the chi-square test was used for comparison of categorical data between groups. The chi-square test was also used to investigate the difference in the distribution of CNVs in the FCGR3 gene between different groups. The age-and sex-adjusted logistic regression model was used to investigate the influence of CNVs on the chronicity of HBV infection. Results There was a significant difference in the frequency distribution of CNVs in the FCGR3A and FCGR3B genes between the chronic HBV infection group and the self-limited HBV infection group ( χ 2 =11.406 and 19.143, both P < 0.05). As for disease progression after chronic HBV infection, there were no significant differences in CNVs of the FCGR3A and FCGR3B genes between the CHB group, the LC group, and the HCC group (FCGR3A: χ 2 =3.125, P =0.537; FCGR3B: χ 2 =5.274, P =0.260). There were also no significant differences in CNVs of the FCGR3A and FCGR3B genes between the HBeAg-positive group and the HBeAg-negative group (FCGR3A: χ 2 =1.025, P =0.599; FCGR3B: χ 2 =0.712, P =0.701). Reduction or deletion of the copy number of the FCGR3A and FCGR3B genes was a risk factor for the chronicity of HBV infection (FCGR3A: odds ratio [ OR ]=0.621, 95% confidence interval [ CI ]: 0.513-0.752; FCGR3B: OR =0.594, 95% CI : 0.491-0.719). Conclusion Reduction or deletion of the copy number of the FCGR3A and FCGR3B genes may be a genetic susceptibility factor for the chronicity of HBV infection, but it is not associated with disease progression.
