Additionally, infection of MDMs with HIV-1 budding-deficient mutant (PTAP-)12, CA-mutants deficient for Gag–Gag interaction13, and cyclophilin A (CyPA)-binding-deficient CA mutant G89V (Supplementary Fig. 2c, f, i) resulted in upregulation of CD169 and IP-10 (Supplementary Fig. 2d, e, g, h, j, k), suggesting that neither virion-release14, cytoplasmic accumulation of higher-ordered Gag assembly intermediates nor CyPA-binding to de novo expressed Gag, a target of a cryptic sensor in myeloid dendritic cells11, is required for MDM activation. The gene discussed is PPIA; the disease is infection.