Extracellular Vesicles from Trypanosoma brucei Mediate Virulence Factor Transfer and Cause Host Anemia | Zendy

Anthony J. Szempruch | Zendy; Steven E. Sykes | Zendy; Rudo Kieft | Zendy; Lauren Dennison | Zendy; A. Becker | Zendy; Anzio Gartrell | Zendy; William J. Martin | Zendy; Ernesto Nakayasu | Zendy; Igor C. Almeida | Zendy; Stephen L. Hajduk | Zendy; John M. Harrington | Zendy

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Extracellular Vesicles from Trypanosoma brucei Mediate Virulence Factor Transfer and Cause Host Anemia

Author(s) -

Anthony J. Szempruch,

Steven E. Sykes,

Rudo Kieft,

Lauren Dennison,

A. Becker,

Anzio Gartrell,

William J. Martin,

Ernesto Nakayasu,

Igor C. Almeida,

Stephen L. Hajduk,

John M. Harrington

Publication year - 2016

Publication title -

cell

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 26.304

H-Index - 776

eISSN - 1097-4172

pISSN - 0092-8674

DOI - 10.1016/j.cell.2015.11.051

Subject(s) - biology , trypanosoma brucei , virulence , extracellular vesicles , virulence factor , host (biology) , extracellular , trypanosoma , microbiology and biotechnology , extracellular vesicle , host factor , vesicle , equine infectious anemia , virology , microvesicles , genetics , gene , virus , microrna , membrane

Intercellular communication between parasites and with host cells provides mechanisms for parasite development, immune evasion, and disease pathology. Bloodstream African trypanosomes produce membranous nanotubes that originate from the flagellar membrane and disassociate into free extracellular vesicles (EVs). Trypanosome EVs contain several flagellar proteins that contribute to virulence, and Trypanosoma brucei rhodesiense EVs contain the serum resistance-associated protein (SRA) necessary for human infectivity. T. b. rhodesiense EVs transfer SRA to non-human infectious trypanosomes, allowing evasion of human innate immunity. Trypanosome EVs can also fuse with mammalian erythrocytes, resulting in rapid erythrocyte clearance and anemia. These data indicate that trypanosome EVs are organelles mediating non-hereditary virulence factor transfer and causing host erythrocyte remodeling, inducing anemia.

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