Previous reports have shown that IP-10 both contributes to activation-independent apoptosis (p38-mediated) of primary human T cells and becomes elevated in the context of chronic hepatitis C virus infection, leading to the sensitization of primary human CD4+ and CD8+ T cells to activation-induced apoptosis (Sidahmed et al., 2012; Zhao et al., 2013). Here, CXCL10 is linked to chronic hepatitis C virus infection.