Coinfection with Hepatitis C Virus among HIV-1-Infected Individuals Increases Proinflammatory Cytokines and HIV-1 Disease Severity

However, in cases of HIV-1 and HCV coinfection, the number of chronic HCV infections rises to 90% [4]. The result of any viral infection depends on the interplay between the activation of host cellular factors to the infection and the viral mechanisms that counteract them [5]. HCV is responsible for activating antiviral interferon (IFN)-α/β expression, but irrespective of the expression of these cytokines, HCV can still replicate within the liver [6]. This could be due to the fact that the nonstructural proteins, nonstructural protein (NS)3 and NS5A, and the structural protein E2 can block the expression as well as transcription of IFN-α/β genes. Also, the NS5A protein induces expression of interleukin (IL)-8, associated with IFN-α inhibition [7] HCV can also block the antiviral action of natural killer (NK) and NKT cells thus hindering the expression of IFN-γ (an antiviral cytokine) due to the interaction between E2 and NK-cell CD81 molecule [8]. The production of cytokines by dendritic cells (DCs) is particularly affected by chronic HCV infection and there are contradictory reports concerning the expression of Th1 cytokines, with some studies suggesting that a Th1 response is suppressed [9] and some studies suggesting a progressive liver injury during chronic HCV has been associated with an increase in the Th1 responseassociated cytokines [10]. In this regard, HCV CD4+ T cells also play an important role in providing an adaptive response by activating cytotoxic and humoral responses. This can involve the secretion Volume 4 Issue 1 2016