KYN was up-regulated in patients infected by SFTSV especially in fatal SFTS patients and possibly contributed to the abnormal biological processes, immune disorders and neural disruption during SFTSV infection as the increases of KYN could suppress and induce the apoptosis of Th1 and natural killer cells as well as down-regulate the CD8+ receptor expression, impairing their cytotoxic activity [22]. This evidence concerns the gene CD8A and infection.