Abstract
Background & Objective:Atypical chemokine receptor 1(ACKR1) represents an atypical chemokine receptor that can bind promiscuously to various chemokines. Chemokines play a crucial role to recruit leukocyte subsets migration through the endothelium and into liver against the virus during the progression of hepatitis C virus (HCV) infection. Most HCV positive patients can lead to liver fibrosis. Hyaluronic acid (HA), laminin (LN), collagen IV(C-IV) and amino-terminal pro-peptide of Type-III pro-collagen (PIII NP) are indices of the extent of liver fibrosis. The aim of this study was to investigate the association between ACKR1 polymorphism and liver fibrosis with these four serum liver markers in HCV positive patients.Methods:From April 2015 to December 2015, a total of 210 patients (109 males and 101 females) with chronic HCV infection at Dalian Infectious Hospital were recruited to participate in this study. ACKR1 genotyping was using TaqMan probes method. HA, LN, C-IV and PIII NP were detected by using diagnostic kits.Results:We compared serum levels of HA, LN, C-IV and PIII NP between FY*A/FY*A and FY*A/FY*B patients and the differences were not significant (P=0.905, P=0.298, P=0.880 and P=0.470, respectively).Conclusions:This study has attempted to elucidate the role of ACKR1 polymorphism in liver fibrosis progression of HCV infection, our results demonstrated that ACKR1 polymorphism is not directly associated with the fibrogenesis in HCV positive patients.
Highlights
Hepatitis C virus (HCV) is a global public health problem, which affects 130 to 150 million individuals
Liver fibrosis is resulted from the loss of normal liver cell function due to excess deposition of various components that constitute the extracellular matrix (ECM) involving molecular and histological rearrangement of various types of collagens, proteoglycans, structural glycoproteins and hyaluronic acid (HA).[1]
In order to enrich the knowledge of this field, we aimed to investigate the association between atypical chemokine receptor 1 (ACKR1) polymorphism and liver fibrosis progression with Hyaluronic acid (HA), LN, collagen IV (C-IV) and PIIINP
Summary
Hepatitis C virus (HCV) is a global public health problem, which affects 130 to 150 million individuals. Liver biopsy has many short comings.[2] In recent years, some studies have proposed noninvasive, serum-based biomarkers: HA, laminin (LN), collagen IV (C-IV) and amino-terminal pro-peptide of Type-III pro-collagen (PIIINP) as indices of the extent of liver fibrosis in chronic liver diseases.[3]. Hyaluronic acid (HA), laminin (LN), collagen IV(C-IV) and amino-terminal pro-peptide of Type-III pro-collagen (PIII NP) are indices of the extent of liver fibrosis. The aim of this study was to investigate the association between ACKR1 polymorphism and liver fibrosis with these four serum liver markers in HCV positive patients. Conclusions: This study has attempted to elucidate the role of ACKR1 polymorphism in liver fibrosis progression of HCV infection, our results demonstrated that ACKR1 polymorphism is not directly associated with the fibrogenesis in HCV positive patients
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