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 Pathogjournal_title
PLoS pathogensauthors
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 DPdoi
10.1371/journal.ppat.1007536subject
Has Abstractpub_date
2019-02-04 00:00:00pages
e1007536issue
2eissn
1553-7366issn
1553-7374pii
PPATHOGENS-D-18-01592journal_volume
15pub_type
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