Cellular exhaustion, which has also been explored in both infections, is phenotypically characterized by the expression of inhibitory molecules such as programmed cell death protein 1 (PD-1), cytotoxic T-lymphocyte–associated antigen 4 (CTLA-4), lymphocyte-activation gene 3 (LAG-3), and T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3). Here, HAVCR2 is linked to infection.