SIRT1 and infection: Patients possessed high populations of aberrantly elevated expression of CD38 in CD8+ T lymphocytes, and the high CD38 levels depleted intracellular NAD+ levels resulting in repressed SIRT-1 activity to elevate acetylated status of its substrate EZH2 and consequently impair transcriptional programmes associated with T lymphocyte cytotoxicity response to amplify susceptibility to pathogenic infections (Katsuyama et al., 2020).