The host-hepatitis C virus (HCV) interaction determines whether the acute phase of HCV infection will undergo complete resolution or progress to the development of viral persistence and, ultimately, chronic HCV infection. The host cell mechanism that fights against the virus culminates in the production of interferons (IFNs), IFN-stimulated genes, and cytokines as well as the induction of autophagy and apoptosis. Innate immune responses modulate adaptive immune responses. T cells often fail and the virus persists as a result of T-cell exhaustion and the emergence of viral escape mutations. Exhausted T cells are unable to control the virus infection. A reversal of T-cell exhaustion after treatment with direct-acting antivirals (DAAs), characterized by the enhanced proliferation of HCV-specific CD8+T cells, down-regulates programmed cell death-1 (PD-1) expression and transitions cells towards a TCF-1+CD127+ memory-like T-cell phenotype. The early initiation of treatment with DAAs during the acute phase of HCV infection is important because it reduces immune exhaustion and results in stronger HCV-specific T-cell responses after treatment, thereby reducing the risk of possible reinfection. Furthermore, since the successful treatment of HCV by DAAs does not lead to the complete reversal of T-cell exhaustion, HCV reinfections may occur. Therefore, a prophylactic vaccine is needed to avoid reinfections and achieve the global elimination of HCV infections. This review provides an overview of the current understanding of the pathophysiology behind HCV infection where the current research and treatment are pointing towards.
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