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Viruses. 2019 May 2;11(5). pii: E410. doi: 10.3390/v11050410.

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

Author information

1
Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, VA 20110, USA. mpleet@gmu.edu.
2
Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, VA 20110, USA. cdemarin@gmu.edu.
3
Department, Emergent BioSolutions, Gaithersburg, MD 20879, USA. stoniers@ebsi.com.
4
Virology Division, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702, USA. stoniers@ebsi.com.
5
Virology Division, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702, USA. john.m.dye1.civ@mail.mil.
6
Viral Immunology Section, Neuroimmunology Branch, National Institute for Neurological Disease and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA. jacobsons@ninds.nih.gov.
7
Department. Integrated BioTherapeutics, Inc., Gaithersburg, MD 20850, USA. jaman@integratedbiotherapeutics.com.
8
Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, VA 20110, USA. fkashanc@gmu.edu.

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 affected 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 effects in recipient cells. Furthermore, we discuss some of the effects that may be induced by EBOV EVs that have not yet been characterized and highlight the remaining questions and future directions.

KEYWORDS:

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

Conflict of interest statement

Disclaimer: The views and conclusions contained in this document are those of the authors and should not be interpreted as necessarily representing the official policies, either expressed or implied, of the US Department of the Army, the US Department of Defense, the US Department of Health and Human Services, or of the institutions and companies affiliated with the authors.

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