Ebola Virus VP40 Modulates Cell Cycle and Biogenesis of Extracellular Vesicles.

ABSTRACT:

Background

Ebola virus (EBOV) mainly targets myeloid cells; however, extensive death of T cells is often observed in lethal infections. We have previously shown that EBOV VP40 in exosomes causes recipient immune cell death.

Methods

Using VP40-producing clones, we analyzed donor cell cycle, extracellular vesicle (EV) biogenesis, and recipient immune cell death. Transcription of cyclin D1 and nuclear localization of VP40 were examined via kinase and chromatin immunoprecipitation assays. Extracellular vesicle contents were characterized by mass spectrometry, cytokine array, and western blot. Biosafety level-4 facilities were used for wild-type Ebola virus infection studies.

Results

VP40 EVs induced apoptosis in recipient T cells and monocytes. VP40 clones were accelerate

SUBMITTER: Pleet ML 

PROVIDER: S-EPMC6249571 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature