Extracellular vesicles from Kaposi Sarcoma-associated herpesvirus lymphoma induce long-term endothelial cell reprogramming.

Abstract:

:Extracellular signaling is a mechanism that higher eukaryotes have evolved to facilitate organismal homeostasis. Recent years have seen an emerging interest in the role of secreted microvesicles, termed extracellular vesicles (EV) or exosomes in this signaling network. EV contents can be modified by the cell in response to stimuli, allowing them to relay information to neighboring cells, influencing their physiology. Here we show that the tumor virus Kaposi's Sarcoma-associated herpesvirus (KSHV) hijacks this signaling pathway to induce cell proliferation, migration, and transcriptome reprogramming in cells not infected with the virus. KSHV-EV activates the canonical MEK/ERK pathway, while not alerting innate immune regulators, allowing the virus to exert these changes without cellular pathogen recognition. Collectively, we propose that KSHV establishes a niche favorable for viral spread and cell transformation through cell-derived vesicles, all while avoiding detection.

journal_name

PLoS Pathog

journal_title

PLoS pathogens

authors

McNamara RP,Chugh PE,Bailey A,Costantini LM,Ma Z,Bigi R,Cheves A,Eason AB,Landis JT,Host KM,Xiong J,Griffith JD,Damania B,Dittmer DP

doi

10.1371/journal.ppat.1007536

subject

Has Abstract

pub_date

2019-02-04 00:00:00

pages

e1007536

issue

2

eissn

1553-7366

issn

1553-7374

pii

PPATHOGENS-D-18-01592

journal_volume

15

pub_type

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