To understand to what extent findings from murine experiments concerning T cell exhaustion in the LCMV model translate to humans, hepatitis C infection is the ideal model that can provide an understanding of TOX expression and cooperation with other transcription factors and correlation with immune checkpoint molecules, activation, and differentiation markers during acute, chronic, and post-resolution of viral infection and different levels of antigen exposure (36, 37). This evidence concerns the gene TOX and hepatitis C virus infection.