Abstract

ABSTRACTAimElucidating differences in gene expression may be useful in understanding the molecular pathogenesis and for developing specific markers for the outcome of hepatitis B virus (HBV) infection. In the present study, expressions of host gene interferon gamma-inducible protein (IP-10), p53, and Foxp3 were studied in hepatocytes of patients with chronic HBV infection to determine a possible link between selected host gene expression and the outcome of HBV infection.Materials and methodsThe study was conducted in 60 patients with chronic HBV infection and they were divided into four groups: HBV-positive cirrhosis (n = 15), HBV-negative cirrhosis (n = 15), HBV-positive hepatocellular carcinoma (HCC) (n = 15) and HBV-negative HCC (n = 15). Total messenger ribonucleic acid (mRNA) extraction was done followed by complementary deoxyribonucleic acid (cDNA) synthesis, and finally gene expression was performed using real-time polymerase chain reaction (PCR) technique.ResultsIP-10 and p53 gene expressions were lower in HBV-positive cirrhosis, and Foxp3 gene expression was upregulated in HBV-positive cirrhosis in comparison to HBV-negative cirrhosis. The expressions of all the three genes were upregulated among HBV-positive HCC in comparison to HBV-negative HCC. The expression of IP-10, p53, and Foxp3 genes was upregulated in HBV-positive HCC in comparison to HBV-positive cirrhosis.ConclusionThis study indicates that there are variations in the expression of the selected genes among cirrhosis and HCC patients with or without HBV. All the three selected genes were more or less upregulated in HBV-positive HCC patients, but only Foxp3 expression was upregulated in HBV-positive cirrhosis. These three particular genes may have a role in the molecular pathogenesis and clinical outcome of HBV-positive cirrhosis and HCC patients. These aspects need further evaluation by studies with larger numbers of cirrhosis and HCC patients.How to cite this articleShahera U, Munshi S, Jahan M, Nessa A, Alam S, Tabassum S. IP-10, p53, and Foxp3 Expression in Hepatocytes of Chronic Hepatitis B Patients with Cirrhosis and Hepatocellular Carcinoma. Euroasian J Hepato-Gastroenterol 2016;6(2):149-153.

Highlights

  • Hepatitis B virus (HBV) is a noncytopathic, hepatotropic deoxyribonucleic acid (DNA) virus which is capable of inducing acute and chronic necro-inflammatory liver injury.[1]

  • IP-10 and p53 gene expressions were lower in HBV-positive cirrhosis, and Foxp[3] gene expression was upregulated in HBV-positive cirrhosis in comparison to HBV-negative cirrhosis

  • This study indicates that there are variations in the expression of the selected genes among cirrhosis and hepatocellular carcinoma (HCC) patients with or without HBV

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Summary

Introduction

Hepatitis B virus (HBV) is a noncytopathic, hepatotropic deoxyribonucleic acid (DNA) virus which is capable of inducing acute and chronic necro-inflammatory liver injury.[1] More than 350 million people worldwide are chronically infected with HBV, causing acute and chronic necro-inflammatory liver injury and promoting hepatocarcinogenesis.[2] chronic HBV infection causes liver cirrhosis (LC) leading to hepatocellular carcinoma (HCC), estimated over 50% of all HCC cases worldwide.[3] Every year about one million people die of HBV-related cirrhosis or HCC.[4]. A strong genetic component with modified gene expression seems to be the major driving force affecting the course of viral hepatitis.[5] Differential host gene regulation contributes to the different outcomes of HBV infection. Both virological and host immunological factors play important roles in determining

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