| Background Hepatitis B virus(HBV) infection is an epidemic disease worldwide and it is also a major infectious disease threatening human health globally. Hepatitis B surface antigen(HBs Ag) is a gold-standard marker for diagnosis of HBV infection. Mathematical modeling of the decline in HBs Ag expression following treatment has been used to predict the therapy required for HBs Ag seroconversion for both PEGylated-interferon alpha-2a and nucleotide/nucleoside analog-based therapies. Recently, several studies reported that the expression of HBs Ag were no associated with Fibrosis in liver and the expression of HBc Ag were highly associated with Fibrosis in liver. But the relation ship between the epression of HBs Ag and HBc Ag in liver and serum level was too few. This article was to analyze the relationships between HBs Ag expression in hepatocytes and serum HBs Ag levels, to understanding this relationship will provide insights into the mechanisms of HBs Ag synthesis and secretion in the different phases of chronic HBV infection and expresion and clinical study of intrahepatic hepatitis B core antigen in patients with chronic hepatitis B.Method The 302 patients were recruited from January 2014 to January 2015 in the Department of Infectious Diseases of The First Affiliated Hospital, Anhui Medical University. Serum HBV DNA HBs Ag, anti-HBs, HBe Ag, anti-HBe, anti-HBc and Liver stiffness were tested in the same day with liver biopsies aims to maximize the liver puncture synchronization. While using immunohistochemical SP method to detect the expression of HBs Ag and HBc Ag, Five horizons were selected at random, with 100 liver cells selected from each horizon, and counted the number of positive cells.Result(1) Median HBs Ag expression was significantly higher in HBe Ag-positive patients as compared to HBe Ag-negative(P = 0.002). there was no significant correlation between the levels of histologic activity associated with the stages of fibrosis(S) and inflammation grade(G), and HBs Ag expression levels in hepatocytes(all P > 0.05), however, the serum HBV DNA levels correlated with the levels of S and G(all P < 0.05)(2) Correlations were observed between serum HBs Ag titers and HBs Ag expression in hepatocytes according to HBe Ag status(HBe Ag-positive: r = 0.051, P = 0.557; HBe Ag-negative: r = 0.377, P < 0.001;). Regardless of HBe Ag status in patients(positive or negative), HBV-DNA levels showed no significant correlation with HBs Ag expression in hepatocytes(all P > 0.05), however, HBe Ag-positive patients did correlate with serum HBs Ag titers(r = 0.569, P < 0.001). For HBe Ag-negative patients, HBV DNA levels did not correlate with serum HBs Ag titers(r = 0.110, P = 0.157)(3) The correlation between serum HBs Ag levels and HBs Ag expression in hepatocytes during the phases of chronic HBV infection increased along with phase progression(immune tolerance: r =-0.184, P = 0.238; immune clearance: r = 0.068, P = 0.722; Immune control: r = 0.496, P = 0.012; and Immune escape: r = 0.575, P = 0.002)(4) The expression of HBc Ag in liver tissue was significantly correlated with the level of serum HBV DNA, HBs Ag, HBe Ag, and Fibroscan in S2-3 group(p<0.05=, but there was no significant correlation in S1 group(p > 0.05)Conclusion The correlation between serum HBs Ag levels and HBs Ag expression in hepatocytes during the immune-tolerant, immune-clearance, Immune control and Immune escape phases of HBV-infected patients gradually increased(r =-0.184, 0.068, 0.492, and 0.575; and P = 0,238, 0,722, 0.012, and 0.002, respectively). These results may indicated that different mechanisms may be involved in HBs Ag synthesis and secretion during various phases of chronic HBV infection andthere is a certain relevance with the expression of HBc Ag in liver cells and the serum levels of HBV DNA, HBs Ag, HBe Ag and Fibroscan, and the specific mechanism needs further studied. |
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