Although T cells from both diseases express high levels of genes encoding for inflammatory proteins and chemokines, COVID-19 subsets expressed high levels of GZMB and CXC3CR1 (Figure 5E), suggesting increased cytotoxicity and terminal effector function, while HIV-1 subsets showed upregulation of CXCR4 and TNFAIP3, which modulate cell proliferation and initiate inflammatory immune responses, respectively. Here, TNFAIP3 is linked to COVID-19.