The most striking effect was observed with a SAMHD1 C-terminal deletion variant, SAMHD1(1–595), which was unable to efficiently inhibit HIV-1 infection (Fig. 1D), even when expressed at levels similar to those at which full-length SAMHD1 suppressed HIV-1 infection by more than 100-fold. Here, SAMHD1 is linked to HIV-1 infection.