Objective:To investigate the correlation of mRNA expression levels and DNA methylation levels of Alu-mediated p21 transcriptional regulator (APTR) with hepatitis B virus infection.Methods:One hundred patients with HBV infection admitted in Affiliated Hospital of Yunnan University during January to December 2019 were enrolled in the study, including 50 patients with chronic hepatitis B (CHB group) and 50 asymptomatic HBV carriers (ASC group); and 50 healthy subjects were also enrolled as the healthy control group. The DNA methylation levels of APTR gene were detected by methylation-sensitive high-resolution melting (MS-HRM); the expression levels of APTR mRNA were detected by fluorescence real-time quantitative PCR (qRT-PCR). Pearson correlation or Spearman rank correlation was used for correlation analysis.Results:There were significant differences in the APTR DNA methylation levels among the CHB, ASC and healthy control groups {[12.02 (9.30, 23.32)]%, [10.02 (8.46, 17.44)]% and [8.86 (7.82, 11.57)]%, χ2=13.360, P<0.01}. The APTR DNA methylation levels were significantly higher in CHB group than those in healthy control group( Z=31.480, P<0.01). There were significant differences in the APTR mRNA expression levels among CHB, ASC and healthy control groups (2.38±1.41, 5.78±2.78 and 5.70±2.66, F=33.720, P<0.01). The APTR mRNA expression levels were significantly lower in CHB group than those in healthy control and ASC groups ( t=7.808 and 7.724, both P<0.01). Correlation analysis showed that the DNA methylation level of APTR gene was negatively correlated with mRNA expression levels ( r=-0.305, P<0.01) in all subjects. The DNA methylation level of APTR gene was positively correlated with HBsAg level ( r=0.231, P=0.022), and the mRNA expression level was negatively correlated with HBsAg level ( r=-0.245, P=0.014) in patients with HBV infection. Conclusion:There are differences in DNA methylation and mRNA expression of APTR gene in different stages of HBV infection, suggesting that APTR gene may be involved in the immune regulation of HBV infection.