Research Article Impact of IFN-Free and IFN-Based Treatment on Blood Myeloid Dendritic Cell, Monocyte, Slan-DC, and Activated T Lymphocyte Dynamics during HCV Infection Serena Vita , 1,2 Paola Zuccalà, 1 Stefano Savinelli, 1 Claudia Mascia, 1 Raffaella Rossi, 1 Francesco Schiavone, 3 Raffaella Marocco, 2 Tiziana Tieghi, 2 Marco Iannetta, 1 Parni Nijhawan, 1 Maria Antonella Zingaropoli, 1 Gabriella d’Ettore, 1 Vincenzo Vullo, 1 Claudio Maria Mastroianni , 1 and Miriam Lichtner 1 1 Department of Public Health and Infectious Disease, Sapienza University of Rome, Italy 2 S.M. Goretti Hospital, Latina, Italy 3 Department of Molecular Medicine, Sapienza University of Rome, Italy Correspondence should be addressed to Serena Vita; serena.vita@gmail.com Received 23 May 2019; Revised 20 December 2019; Accepted 24 February 2020; Published 16 March 2020 Academic Editor: Martin Holland Copyright © 2020 Serena Vita et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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. 1. Introduction 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), macro- phages, dendritic cells (DCs), and T cells [4–8]. As a result of this, the expression profile of circulating pro- and anti- inflammatory cytokines and chemokines is altered, leading to chronic infection and persistent inflammation [4–8]. 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 geno- types [9–11]. IFN-α has antiviral activity and also enhances HCV-specific T cell responses; ribavirin, a nucleoside ana- logue, 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]. In recent years, the introduction of several oral IFN-free direct-acting antiviral agents (DAAs) in clinical practice has proved to be a milestone in the management of HCV infec- tion, increasing sustained virological response (SVR) rates up to 95-100% [13]. DAAs are molecules that target specific nonstructural proteins of the virus, with subsequent disrup- tion of viral replication and spread to other cells. Since IFN-free DAA regimens specifically target various steps in the HCV life cycle, they can provide the opportunity to eluci- date the relationship between HCV and the innate immune response, without the confounding effect of the IFN-α- induced immune modulation. Hindawi Journal of Immunology Research Volume 2020, Article ID 2781350, 11 pages https://doi.org/10.1155/2020/2781350