Extracellular Vesicles and Ebola Virus: A New Mechanism of Immune Evasion



Viruses


Abstract: Ebola virus (EBOV) disease can result in a range of symptoms anywhere from virtually asymptomatic to severe hemorrhagic fever during acute infection. Additionally, spans of asymptomatic persistence in recovering survivors is possible, during which transmission of the virus may occur. In acute infection, substantial cytokine storm and bystander lymphocyte apoptosis take place, resulting in uncontrolled, systemic inflammation in a ected individuals. Recently, studies have demonstrated the presence of EBOV proteins VP40, glycoprotein (GP), and nucleoprotein (NP) packaged into extracellular vesicles (EVs) during infection. EVs containing EBOV proteins have been shown to induce apoptosis in recipient immune cells, as well as contain pro-inflammatory cytokines. In this manuscript, we review the current field of knowledge on EBOV EVs including the mechanisms of their biogenesis, their cargo and their e ects in recipient cells. Furthermore, we discuss some of the e ects that may be induced by EBOV EVs that have not yet been characterized and highlight the remaining questions and future directions.


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Keywords: Ebola virus; exosome; extracellular vesicles; VP40; NP; GP; cytokine

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