Innate sensing of HIV-1 assembly by Tetherin induces NFκB-dependent proinflammatory responses.

ABSTRACT: Antiviral proteins that recognize pathogen-specific or aberrantly located molecular motifs are perfectly positioned to act as pattern-recognition receptors and signal to the immune system. Here we investigated whether the interferon-induced viral restriction factor tetherin (CD317/BST2), which is known to inhibit HIV-1 particle release by physically tethering virions to the cell surface, has such a signaling role. We find that upon restriction of Vpu-defective HIV-1, tetherin acts as a virus sensor to induce NFκB-dependent proinflammatory gene expression. Signaling requires both tetherin's extracellular domain involved in virion retention and determinants in the cytoplasmic tail, including an endocytic motif, although signaling is independent of virion endocytosis. Furthermore, recruitment

SUBMITTER: Galao RP 

PROVIDER: S-EPMC3556742 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature