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.
journal_name
PLoS Pathogjournal_title
PLoS pathogensauthors
Assil S,Futsch N,Décembre E,Alais S,Gessain A,Cosset FL,Mahieux R,Dreux M,Dutartre Hdoi
10.1371/journal.ppat.1007589subject
Has Abstractpub_date
2019-02-28 00:00:00pages
e1007589issue
2eissn
1553-7366issn
1553-7374pii
PPATHOGENS-D-18-01563journal_volume
15pub_type
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