CD38 and hepatitis A virus infection: Interferon-independent robust CXCL10 production (22) and T cell receptor-independent activation of CD8+ T cell (23) have been suggested as mechanisms for innate-like cytotoxicity in patients with hepatitis A. In addition, innate-like bystander-activated CD38+HLA-DR+CD8+ T cells are known to play a pathogenic role in patients with chronic hepatitis C (24).