Fig. 6.

ITIM phosphorylation is required for the Vif–SHP-1 interaction and cytokine inhibition. A ITIM mutants of HA–Vif and GST–Vif. B Immunoassay of lysates of HEK293T cells expressing various vectors. C Direct binding of GST–Vif or its ITIM mutant to His–SHP-1 (left) or endogenous SHP-1 from THP-1 cells (right). D IFNB, CXCL10, ISG15, and TNF mRNA levels in MDMs infected with HIV-1, HIV-1ΔVif, or HIV-1-Vif(Y147F) for 24 h (n = 3). E Immunoblot of lysates of MDMs infected with HIV-1, HIV-1ΔVif, or HIV-1-Vif(Y147F). F ELISA of IFN-β and TNF in supernatants from (D) (n = 3). G Tat-Rev mRNA expression in MDMs infected with HIV-1, HIV-1ΔVif, or HIV-1-Vif(Y147F) for 24 h (n = 3). H Immunoblot of lysates of THP-1 cells infected with HIV-1, HIV-1ΔVif, or HIV-1-Vif(Y147F). I Immunoassay of lysates of THP-1 cells infected with HIV-1, HIV-1ΔVif, or HIV-1-Vif(Y147F). J Immunoblot (native PAGE) demonstrating STING dimerization in THP-1 cells infected with HIV-1, HIV-1ΔVif, or HIV-1-Vif(Y147F). The data are representative of at least three independent experiments. The data are the means ± SEMs. ***P < 0.001 (two-tailed unpaired Student’s t test)