Next Article in Journal
New Bacteriophages against Emerging Lineages ST23 and ST258 of Klebsiella pneumoniae and Efficacy Assessment in Galleria mellonella Larvae
Next Article in Special Issue
Cytokine Effects on the Entry of Filovirus Envelope Pseudotyped Virus-Like Particles into Primary Human Macrophages
Previous Article in Journal
IIV-6 Inhibits NF-κB Responses in Drosophila
Previous Article in Special Issue
Inflammatory and Humoral Immune Response during Ebola Virus Infection in Survivor and Fatal Cases Occurred in Sierra Leone during the 2014–2016 Outbreak in West Africa
Open AccessReview

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

1
Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, VA 20110, USA
2
Emergent BioSolutions, Gaithersburg, MD 20879, USA
3
Virology Division, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702, USA
4
Viral Immunology Section, Neuroimmunology Branch, National Institute for Neurological Disease and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA
5
Integrated BioTherapeutics, Inc., Gaithersburg, MD 20850, USA
*
Author to whom correspondence should be addressed.
Viruses 2019, 11(5), 410; https://doi.org/10.3390/v11050410
Received: 29 March 2019 / Revised: 29 April 2019 / Accepted: 1 May 2019 / Published: 2 May 2019
(This article belongs to the Collection Advances in Ebolavirus, Marburgvirus, and Cuevavirus Research)
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. View Full-Text
Keywords: Ebola virus; exosome; extracellular vesicles; VP40; NP; GP; cytokine Ebola virus; exosome; extracellular vesicles; VP40; NP; GP; cytokine
Show Figures

Figure 1

MDPI and ACS Style

Pleet, M.L.; DeMarino, C.; Stonier, S.W.; Dye, J.M.; Jacobson, S.; Aman, M.J.; Kashanchi, F. Extracellular Vesicles and Ebola Virus: A New Mechanism of Immune Evasion. Viruses 2019, 11, 410. https://doi.org/10.3390/v11050410

AMA Style

Pleet ML, DeMarino C, Stonier SW, Dye JM, Jacobson S, Aman MJ, Kashanchi F. Extracellular Vesicles and Ebola Virus: A New Mechanism of Immune Evasion. Viruses. 2019; 11(5):410. https://doi.org/10.3390/v11050410

Chicago/Turabian Style

Pleet, Michelle L.; DeMarino, Catherine; Stonier, Spencer W.; Dye, John M.; Jacobson, Steven; Aman, M. J.; Kashanchi, Fatah. 2019. "Extracellular Vesicles and Ebola Virus: A New Mechanism of Immune Evasion" Viruses 11, no. 5: 410. https://doi.org/10.3390/v11050410

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop