CD4 and infection: We showed that IFNα secreting pDC compensated for HIV inhibition of IFN-I production in its target cells in two different ways: i) reduced infection in DCs and macrophages which would limit viral spread to resident or newly infiltrating memory CD4 T cells; ii) reactivation of latent HIV in all subsets of resting memory CD4 T cell subsets, accompanied by limited viral spread, upregulation of MHC-I and induction of a tissue retention phenotype.