Abstract
Chronic hepatitis C virus infection leads to the activation of innate immunity, a key component in HCV fibrosis. In the past, the use of IFN-based treatment regimens did not permit an adequate evaluation of the impact of HCV clearance on immune cells, because of their antiviral and immunomodulatory properties. The recent development of direct-acting antiviral (DAA) therapy, which is associated with high rates of sustained virological response, enables a more accurate analysis of the immunological modifications following HCV eradication. We studied the dynamics of blood myeloid dendritic cells, monocytes, slan-DCs, and T lymphocytes during IFN-free and IFN-based regimens in hepatitis C virus infection.
Highlights
Worldwide, an estimated 71 million people are chronically infected with hepatitis C virus (HCV) [1].Chronic HCV infection is characterized by an aberrant inflammatory response that causes HCV-mediated liver damage, leading to progressive fibrosis, potentially resulting in cirrhosis, liver failure, and hepatocarcinoma (HCC) [2, 3].HCV can counteract both innate and adaptive immune responses by modulating the function of several types of cells of the immune system, including monocytes (Mo), macrophages, dendritic cells (DCs), and T cells [4,5,6,7,8]
We stained the plasmacytoid DCs (pDCs) of 5 healthy donors in parallel with both the antibody panel used in our study and a new panel, which included BDCA-2, CD123, and HLA-DR, and we found that the two methods were equivalent
Treatment with telaprevir and boceprevir was intended for genotype 1 HCV-infected patients and antiviral potency was counteracted by considerable side effects, in particular an increased number of bacterial infections [17, 18]
Summary
An estimated 71 million people are chronically infected with hepatitis C virus (HCV) [1].Chronic HCV infection is characterized by an aberrant inflammatory response that causes HCV-mediated liver damage, leading to progressive fibrosis, potentially resulting in cirrhosis, liver failure, and hepatocarcinoma (HCC) [2, 3].HCV can counteract both innate and adaptive immune responses by modulating the function of several types of cells of the immune system, including monocytes (Mo), macrophages, dendritic cells (DCs), and T cells [4,5,6,7,8]. An estimated 71 million people are chronically infected with hepatitis C virus (HCV) [1]. Chronic HCV infection is characterized by an aberrant inflammatory response that causes HCV-mediated liver damage, leading to progressive fibrosis, potentially resulting in cirrhosis, liver failure, and hepatocarcinoma (HCC) [2, 3]. Until August 2011, the commercially available treatment options for HCV infection were limited to interferon-alpha(IFN-α-) based therapies and ribavirin (RBV) for all genotypes [9,10,11]. IFN-α has antiviral activity and enhances HCV-specific T cell responses; ribavirin, a nucleoside analogue, has a small direct activity against HCV but reduces hepatic inflammation [12]. It has been speculated that these two drugs act by modulating the immune system for HCV elimination [12]
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