The Genetic Profile and Serum Level of IL-8 Are Associated with Chronic Hepatitis B and C Virus Infection.

Ednelza Da Silva Graça Amoras,Ricardo Ishak,Simone Regina Souza Da Silva Conde,William Botelho De Brito,Antonio Carlos Rosário Vallinoto,Maria Alice Freitas Queiroz,Izaura Maria Vieira Cayres Vallinoto

doi:10.3390/biom11111664

Abstract

The present study evaluated the IL8-251 A/T polymorphism in samples from 74 patients with chronic hepatitis B (HBV), 100 patients with chronic hepatitis C (HCV), and 300 healthy donors (CG). The correlations of this polymorphism with plasma IL-8 and disease stage were calculated. Polymorphisms were identified by real-time PCR. IL-8 was measured by enzyme-linked immunosorbent assay. The IL8-251 A/T genotype was not associated with susceptibility to infection by HBV or HCV. The wild-type allele (A) was associated with higher levels of inflammation (p = 0.0464) and fibrosis scores (p = 0.0016) in the HBV group, representing an increased risk for increased inflammatory activity (OR = 1.84; p = 0.0464) and for high fibrosis scores (OR = 2.63; p = 0.0016). Viral load was higher in HBV patients with polymorphic genotypes (TA and TT) at the IL8-251 A/T polymorphism than in those with the wild-type genotype (p = 0.0272 and p = 0.0464, respectively). Plasma IL-8 was higher among patients infected with HBV or HCV than in the control group (p = 0.0445 and p = 0.0001, respectively). The polymorphic genotype was associated with lower IL-8 than the wild-type genotype in the HBV group (p = 0.0239) and the HCV group (p = 0.0372). The wild-type genotype for IL8-251 A/T and high IL-8 were associated with a worse prognosis for infections; therefore, they may contribute to viral persistence and the development of more severe forms of chronic viral liver diseases.

Highlights

The hepatic lesion triggered by the hepatitis B and C viruses is mediated mainly by host immune responses to viral proteins expressed in infected hepatocytes and, to a lesser extent, by direct cytopathic effects of viruses [1]
The immune system has adapted to reduce the liver damage caused by immune responses to infectious agents, the infection caused by the hepatitis B virus (HBV)
The objective of this study was to investigate the association of the IL8-251 A/T polymorphism with changes in the plasma level of IL-8, which might influence the progression of chronic diseases caused by HBV and hepatitis C virus (HCV)

Summary

Introduction

The hepatic lesion triggered by the hepatitis B and C viruses is mediated mainly by host immune responses to viral proteins expressed in infected hepatocytes and, to a lesser extent, by direct cytopathic effects of viruses [1]. In this condition, inflammation and tissue remodeling and repair processes occur simultaneously. With persistent injury, this repair process becomes pathological, characterized by extracellular matrix (ECM) deposition, parenchymal cell death, and angiogenesis, together with tissue remodeling [4]. The persistent production of growth factors for HSCs, fibrogenic cytokines, and chemokines by various types of liver cells is involved in fibrogenesis and chronic inflammation [5]. This scar matrix typically accumulates very slowly, but once cirrhosis is established, the potential to reverse this process is diminished and complications develop [3]. Knowledge of the stage of liver fibrosis provides essential information for the prognosis and helps to determine whether antiviral therapy is necessary, in addition to allowing for differential diagnosis with other liver diseases [6]

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