Abstract
Human T Lymphotropic virus (HTLV) infection can persist in individuals resulting, at least in part, from viral escape of the innate immunity, including inhibition of type I interferon response in infected T-cells. Plasmacytoid dendritic cells (pDCs) are known to bypass viral escape by their robust type I interferon production. Here, we demonstrated that pDCs produce type I interferons upon physical cell contact with HTLV-infected cells, yet pDC activation inversely correlates with the ability of the HTLV-producing cells to transmit infection. We show that pDCs sense surface associated-HTLV present with glycan-rich structure referred to as biofilm-like structure, which thus represents a newly described viral structure triggering the antiviral response by pDCs. Consistently, heparan sulfate proteoglycans and especially the cell surface pattern of terminal β-galactoside glycosylation, modulate the transmission of the immunostimulatory RNA to pDCs. Altogether, our results uncover a function of virus-containing cell surface-associated glycosylated structures in the activation of innate immunity.
Highlights
Human T-Lymphotropic Virus type 1 (HTLV-1) infects over an estimation of 5–10 million people
We demonstrate that Plasmacytoid dendritic cells (pDCs) produce IFN-I upon physical contacts with Human T Lymphotropic virus (HTLV)-infected cells
We show that pDCs sense surface associatedHTLV present with glycan-rich structure, referred to as HTLV-biofilm-like structure
Summary
Human T-Lymphotropic Virus type 1 (HTLV-1) infects over an estimation of 5–10 million people. HTLV-1 provirus is mainly found in CD4+ T-cells, yet infected dendritic cells (DCs) are detected [5,6]. Their function is subsequently altered in vivo [6,7,8], thereby most likely contributing to viral pathogenesis. Type-I interferons (referred to as IFN-I, i.e., IFNα and β) are key mediators of innate immunity They induce the expression of IFN-stimulated genes (ISGs) that suppress viral spread at different stages of the viral cycle, and stimulate the onset of adaptive immune responses. Like virtually all viruses [11], HTLV-1 inhibits several steps of the PRR-induced pathways [12,13,14], and as a consequence, blunts IFN-I induction and signaling [15,16], leading to very limited production of IFN-I by infected cells
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