Sensing of cell-associated HTLV by plasmacytoid dendritic cells is regulated by dense β-galactoside glycosylation.


PLoS Pathog. 2019 Feb 28;15(2):e1007589. doi: 10.1371/journal.ppat.1007589. eCollection 2019 Feb. PMID:30818370


Assil S, Futsch N, Décembre E, Alais S, Gessain A, Cosset FL, Mahieux R, Dreux M, Dutartre H.

Discover OR team  Retroviral oncogenesis led by Renaud Mahieux
Discover VIV team  “Vesicular trafficking, innate response and viruses ” led by Marlène Dreux.


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.


Affiliations des auteurs:

Assil S1, Futsch N1, Décembre E1, Alais S1, Gessain A2, Cosset FL1, Mahieux R1, Dreux M1, Dutartre H1.
1 CIRI-Centre International de Recherche en Infectiologie, Univ Lyon, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, ENS Lyon, Lyon, France.
2 Epidémiologie et Physiopathologie des Virus Oncogènes, Institut Pasteur, Paris France.