Hepatitis C virus (HCV) makes successful strategies to antagonize the host immune responses. A persistent HCV infection leads to chronic hepatitis and eventually causes cirrhosis and hepatocellular carcinoma. Spontaneous clearance of HCV infection is associated with a prompt induction of innate immunity. Host cytokines and innate immune responses play an important role in controlling HCV infection. Innate immune responses modulate adaptive immune responses. The inability of the immune system to eliminate pathogens often results in the development of a persistent viral infection. A persistent HCV infection results from inefficient innate and adaptive immunities with exhausted virus-specific T-cell responses. These responses have recently been shown to play a role in the context of antiviral therapy for chronic HCV infection. Recent introduction of direct acting antiviral (DAA) achieved sustained virological response in a majority of HCV-infected patients. Combination therapy with DAAs exhibiting a high barrier to resistance that target different segments of the HCV life cycle will be associated with a low risk of the emergence of resistance and improved efficacy related to curing HCV infection. Detection of HCV carriers, lack of immunity against reinfection, insufficient access to DAA therapy, uncertainty about the magnitude of viral resistance development, and continued risk for several liver damage are the major hurdle to overcome. Developing a protective vaccine for HCV is an unmet medical necessity. However, efforts to develop an HCV vaccine are hampered by viral factors such as HCV genomic diversity, the cell to cell spread of HCV, a high mutation rate, and the development of infectious lipoviral particles. Because the immune response to an HCV infection is protective, ongoing research to develop a safe and affordable vaccine will provide hope for millions of individuals at risk of HCV infection. Global eradication of HCV will not likely be possible without a robust vaccine.
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