Indeed, in addition to hyper-stimulation of PARPs activity by accumulated DNA damage, that can take place in the acute phase of infection, CD38, a major NAD+ hydrolyzing enzyme, is expected to play a central role in NAD consumption and depletion [100], since it is overexpressed in both HBV- and HCV-specific CD8 T cells in the acute and chronic stages of infection [64,65] (Figure 1). Here, CD8A is linked to infection.