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Ebola VP40 in Exosomes Can Cause Immune Cell Dysfunction.

Michelle L Pleet¹, Allison Mathiesen², Catherine DeMarino¹

¹Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas VA, USA.

Frontiers in Microbiology

|November 23, 2016

Summary

Ebola virus protein VP40, packaged in exosomes, induces immune cell death and RNAi machinery dysregulation. Oxytetracycline treatment may reduce exosome levels, protecting the immune system and improving survival.

Keywords:

EBOV ESCRT Ebola virus VLP VP40 apoptosis exosomes microRNA

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Isolation of Exosomes from the Plasma of HIV-1 Positive Individuals

Isolation of Exosomes from the Plasma of HIV-1 Positive Individuals

Published on: January 5, 2016

Area of Science:

Virology
Immunology
Cell Biology

Background:

Ebola virus (EBOV) causes severe hemorrhagic fever with high mortality.
EBOV can persist in survivors, leading to potential transmission.
Exosomes from virus-infected cells can transfer viral components and alter recipient cell activity.

Purpose of the Study:

To investigate the effects of Ebola virus structural proteins (VP40, GP, NP) and VP40-containing exosomes on immune cells.
To determine how VP40 influences exosome biogenesis and RNA interference (RNAi) machinery.
To explore potential therapeutic strategies targeting exosome release.

Main Methods:

Transfection of cells with Ebola virus proteins (VP40, GP, NP).
Analysis of VP40 packaging into exosomes and their effect on recipient immune cells.
Investigation of RNAi machinery (Dicer, Drosha, Ago 1) regulation by VP40.
Assessment of exosome biogenesis and VP40 phosphorylation.
Treatment of cells with r-Roscovitine and Oxytetracycline.
Development of nanoparticle-based capture of viral proteins.

Main Results:

VP40-transfected cells released VP40-containing exosomes that induced apoptosis in recipient immune cells.
VP40 dysregulated RNAi machinery (Dicer, Drosha, Ago 1) in parental and recipient cells.
VP40 increased levels of ESCRT-II and exosomal marker proteins, regulating exosome biogenesis.
VP40 phosphorylation by Cdk2/Cyclin complexes was reversible with r-Roscovitine.
Oxytetracycline treatment reduced VP40-containing exosome levels.
Novel nanoparticles enabled safe capture of viral proteins, minimizing BSL-4 requirements.

Conclusions:

Exosomes containing VP40 may cause bystander lymphocyte apoptosis, leading to immune system destruction and high viral loads.
Modulating exosome release with drugs like Oxytetracycline could protect the adaptive immune system and improve EBOV survival rates.