Hepatitis C
virus (HCV) is a major causative agent of chronic hepatitis, affecting
approximately 200 million people throughout the world. There is a broad array
of functional impairments of virusspecific T cells including decreased
antiviral cytokine production and cytotoxicity; with impaired proliferative
capacity and arrested stages of differentiation.
In liver
infections, CD81 T cells may show features of cells that did not receive
sufficient help. Thus, in chronic lymphocytic choriomeningitis
virus in mice,
failure to eliminate the virus is associated with “exhausted” T cells that
persist, but do not function.
These cells
express a characteristic surface phenotype, including the markers programmed
cell death 1 (PD- 1), T-cell 3 immunoglobulin and mucin domain containing
protein 3 (TIM-3), and lymphocyte activation gene 3 which are also expressed on
human exhausted T cells.
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