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

PLoS Pathogens
Sonia AssilHélène Dutartre

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.

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Citations

Dec 25, 2019·Retrovirology·Brenda RocamondeHélène Dutartre
Dec 20, 2019·Retrovirology·Ramona MolesGenoveffa Franchini
Mar 21, 2021·Reviews in Medical Virology·Sanaz Ahmadi GhezeldashtSeyed Abdolrahim Rezaee
Nov 26, 2019·Journal of Virological Methods·Renaud Mahieux, Hélène Dutartre

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Methods Mentioned

BETA
glycosylation
flow cytometry
FACS
ELISA
confocal microscopy
glycosylations
FCS
Transfection
reverse transcription-PCR
PCR

Software Mentioned

Graphpad
FlowJo
PRISM
IDEAS
Image J
ImageStream

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