Association of PRKAA1 gene polymorphisms with chronic hepatitis B virus infection in Chinese Han population

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Abstract

Objective Studies have indicated that AMPK play critical roles in the regulation of innate immunity and inflammatory responses. However, the role of the polymorphisms of PRKAA1 gene in immune-response to infectious organisms remains unknown. To evaluate the potential role of PRKAA1/AMPKα1 in the immune-response to HBV, we conducted this case–control study. Methods We recruited 276 patients (145 men and 131 women; average age, 51.6 years) with chronic HBV infection (CHB) and 303 healthy controls (166 men and 137 women; average age, 54.2 years). All the subjects were unrelated individuals of Chinese Han Population. Three SNPs of PRKAA1gene were tested. Results Rs1002424 polymorphism showed significant difference in the allele frequencies, but no difference in the genotype frequencies (allele: p = 0.039411, OR95%CI = 0.783479 [0.621067–0.988362]; genotype: p = 0.104758); rs13361707 polymorphism showed significance in allele analysis, but not in genotype analysis (allele: p = 0.034749, OR95%CI = 1.284303 [1.017958–1.620335]; genotype: p = 0.098027); rs3792822 polymorphism was demonstrated to have significant differences in both genotype and allele frequencies between cases and controls (allele: p = 0.029286, OR95%CI= 0.741519 [0.566439–0.970716]; genotype: p = 0.034560). The haplotype results showed that CTG and TCA in the rs13361707–rs1002424–rs3792822 block were significantly associated with the happening of HBV (CTG: p = 0.036854, OR95%CI = 1.281 [1.015–1.617]; p = 0.030841, OR95%CI = 0.743 [0.568–0.973]). Conclusion These findings suggest that PRKAA1 polymorphisms may contribute to the susceptibility of chronic HBV infection in Chinese Han origin.

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Yuan, J., Zhang, Y., Yan, F. tang, & Zheng, X. (2016). Association of PRKAA1 gene polymorphisms with chronic hepatitis B virus infection in Chinese Han population. Brazilian Journal of Infectious Diseases, 20(6), 564–568. https://doi.org/10.1016/j.bjid.2016.08.003

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