Abstract

Hepatocyte nuclear factors 4 alpha (HNF4α) and 3 beta (HNF3β) are members of a group of liver-enriched transcription factors (LETFs) that play important roles in regulating the replication of hepatitis B virus (HBV) and liver inflammation. However, the relationship of the level of HNF4α and HNF3β with the severity of HBV-infected liver diseases is unclear. In this study, liver tissue samples from different types of HBV patients were collected, and HNF4α and HNF3β expression were detected by immunohistochemistry. The expression of HNF4α was significant higher in patients with severe hepatitis B(SHB) than those with chronic hepatitis B(CHB) and liver cirrhosis(LC) (both P < 0.05), but similar between patients with CHB and LC (P > 0.05). And the expression of HNF3β was similar among patients with CHB, LC and SHB (P > 0.05 for all pairwise comparison). This suggests that the expression level of HNF4α was different in patients with different outcome of HBV infection, high expression level of HNF4α may correlate with occurrence of SHB

Highlights

  • Hepatitis B virus (HBV) infection is a serious global health problem, with 2 billion people infected worldwide [1], and it would lead to various clinical outcomes, ranging from an asymptomatic carrier state to acute or chronic liver disease including chronic hepatitis B (CHB), severe hepatitis B (SHB), liver cirrhosis (LC) and hepatocellular carcinoma(HCC) [2]

  • Outcomes of HBV infection are affected by both virus and host factors [4,5,6,7,8], and evidence have showed that viral replication is mainly correlated to the development or progression of diseases [2,4]

  • One of our previous work suggested that HNF4a and HNF3b likely participated in HBV replication in patients with HBV infection, or that HBV replication may somehow influence the expression of hepatocyte nuclear factor 4alpha (HNF4a) and 3 beta (HNF3b) in the liver [11]

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Summary

Introduction

Hepatitis B virus (HBV) infection is a serious global health problem, with 2 billion people infected worldwide [1], and it would lead to various clinical outcomes, ranging from an asymptomatic carrier state (inactive HBV carrier) to acute or chronic liver disease including chronic hepatitis B (CHB), severe hepatitis B (SHB), liver cirrhosis (LC) and hepatocellular carcinoma(HCC) [2]. HBV infection has become the 10th cause of death worldwide, and approximately 15-40% of those patients with CHB will develop to end-stage liver disease including LC, SHB, or HCC [1]. Outcomes of HBV infection are affected by both virus (such as: virus variation, virus protein, virus genotype, etc.) and host factors (such as: cellular immunity, cytokines, apoptosis, etc.) [4,5,6,7,8], and evidence have showed that viral replication is mainly correlated to the development or progression of diseases [2,4]. Hepatic nuclear factors (HNFs) are a group of important host transcription factors that mainly reside in the liver and regulate numerous liver-expressed genes [10]. The study of HNF in hepatitis B has become a research hotspot

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