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The term “Immune response against HCV” refers broadly to the complex set of host defense mechanisms—both humoral (antibody-mediated) and cellular (T cell-mediated)—that act against hepatitis C virus infection. This includes neutralizing antibodies targeting viral envelope proteins such as E2, which can block viral entry into cells[2], as well as cytotoxic T lymphocytes that recognize epitopes from nonstructural proteins like NS3, NS4a/b, NS5a/b[1]. A robust early neutralizing antibody and T cell response is associated with spontaneous clearance of acute infection; delayed or weak responses often result in chronicity[2]. While these processes are critical for controlling or clearing HCV, “Immune response against HCV” is a biological process rather than a discrete molecular entity or therapeutic target. Therefore, it does not fit standard definitions for drug targets such as receptors, enzymes, transporters, etc., but rather describes an outcome of multiple interacting molecules and pathways within the host’s immune system.
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