Comparative untargeted metabolomics analysis of serum metabolic alterations in patients infected with hepatitis B virus genotypes B and C

Abstract

The clinicopathological characteristics and outcomes of patients infected with hepatitis B virus (HBV) differ between genotypes B and C. However, the potential metabolic mechanisms and differences in certain biological pathways associated with different HBV genotypes remain unclear to date. To obtain a better understanding of the effects of liver diseases caused by HBV genotypes B and C on host metabolism, an untargeted metabolomics analysis was performed to assess the differences among the serum metabolic profiles of healthy controls and patients infected with genotypes B or C. Here, a total of 54 serum samples were obtained from healthy controls and patients with chronic HBV infections caused by genotypes B and C, and the samples were subjected to metabolomics analysis. The serum metabolite profiles were analyzed using an ultrahigh-performance liquid chromatography-quadrupole-time-of-flight/mass spectrometry (UHPLC-Q-TOF/MS)-based untargeted metabolomics approach for identifying the differentially expressed metabolites that were upregulated or downregulated by at least 1.5-foldin the serum samples of patients infected with HBV genotypes B and C. A total of 63 metabolites were found to be differentially expressed between the serum samples of healthy controls and patients infected with HBV genotype B, while 57 metabolites were differentially expressed between the serum samples of healthy controls and patients infected with HBV genotype C. The majority of these metabolites were involved in regulating the bile acid (BA) metabolism pathways. The results also indicated that 8 differentially expressed metabolites can serve as potential metabolic biomarkers for distinguishing between individuals infected with the HBV genotype B and C. Altogether, the untargeted metabolomics analysis revealed that infection with HBV genotypes B and C is associated with different metabolic profiles, and the study provided fundamental information for further detailed investigations of the mechanism underlying metabolic dysregulation in HBV infections.