Sahar Essa
Kuwait University, Kuwait
Title: The Conceivable Influence of Persistent Genotype-4 Hepatitis C Virus Infection on Cellular Immune Subsets before, during and after Pegylated Interferon-α and Ribavirin Therapy
Biography
Biography: Sahar Essa
Abstract
Hepatitis C virus (HCV) infection is a major public health problem with an estimated 3-4 million people infected each year worldwide. 20–30% of individuals acutely infected with HCV will spontaneously clear the virus, with the remaining 70–80% developing persistent HCV infection. The interplay between the virus and host innate and adaptive immune responses determine the outcome of HCV infection (Rauch et al., 2009). The present study aims to determine the level of cellular immune subsets in responders and non-responders HCV-infected patients as a result of the standard treatment (PEG-IFN and ribavirin) and to correlate the results with the major HCV genotypes in Kuwait. Data of the immunophenotyping for cellular subsets include 30 healthy controls and
genotype-4 HCV-infected patients (39 responders vs. 21 non-responders) at baseline and after treatment. The immunophenotyping was evaluated by flow cytometry using antibodies specific to mature T cells, T cytotoxic cells, regulatory T cells, T helper cells, activated T cells, natural killer cells, NKT cells and pan B cells. There were significant differences in the mean values of percentages for T helper cells, T cytotoxic cells, B cells, NK cells, NKT cells and activated T cells between HCV-responder vs. HCV-non-responder patients. Also, significant differences were noticed in the mean values of the absolute counts for T helper cells, B cells, NK cells, and T cells. Cellular subsets of the immune system play an important role in the pathogenesis, progression, and clearance of HCV. The screening for multiple cellular markers in the present study showed significant variations in the absolute counts and percentages of essential immune cellular subsets. These findings could lead to new possibilities for immune-based interventions and/or vaccine development with the aim of restoring functional antiviral T cell responses combined with improved viral clearance