دورية أكاديمية
Ebola Virus VP40 Modulates Cell Cycle and Biogenesis of Extracellular Vesicles.
| العنوان: | Ebola Virus VP40 Modulates Cell Cycle and Biogenesis of Extracellular Vesicles. |
|---|---|
| المؤلفون: | Pleet ML; Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, Virginia., Erickson J; Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, Virginia., DeMarino C; Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, Virginia., Barclay RA; Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, Virginia., Cowen M; Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, Virginia., Lepene B; Ceres Nanosciences, Inc., Manassas, Virginia., Liang J; Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland., Kuhn JH; Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, Frederick, Maryland., Prugar L; Virology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, Maryland., Stonier SW; Virology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, Maryland., Dye JM; Virology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, Maryland., Zhou W; Center for Applied Proteomics and Molecular Medicine, George Mason University, Manassas, Virginia., Liotta LA; Center for Applied Proteomics and Molecular Medicine, George Mason University, Manassas, Virginia., Aman MJ; Integrated BioTherapeutics, Inc., Gaithersburg, Maryland., Kashanchi F; Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, Virginia. |
| المصدر: | The Journal of infectious diseases [J Infect Dis] 2018 Nov 22; Vol. 218 (suppl_5), pp. S365-S387. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S. |
| اللغة: | English |
| بيانات الدورية: | Publisher: Oxford University Press Country of Publication: United States NLM ID: 0413675 Publication Model: Print Cited Medium: Internet ISSN: 1537-6613 (Electronic) Linking ISSN: 00221899 NLM ISO Abbreviation: J Infect Dis Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Jan. 2011- : Oxford : Oxford University Press Original Publication: 1904-2010 : Chicago, IL : University of Chicago Press |
| مواضيع طبية MeSH: | Cell Cycle/*physiology , Ebolavirus/*metabolism , Extracellular Vesicles/*metabolism , Hemorrhagic Fever, Ebola/*metabolism , Hemorrhagic Fever, Ebola/*virology , Nucleoproteins/*metabolism , Viral Core Proteins/*metabolism, Apoptosis/physiology ; Cell Line ; Cell Line, Tumor ; Cyclin D1/metabolism ; Exosomes/metabolism ; Extracellular Vesicles/virology ; Glycoproteins/metabolism ; HEK293 Cells ; Humans ; Promoter Regions, Genetic/physiology ; Protein Binding/physiology ; U937 Cells ; Up-Regulation/physiology ; Viral Matrix Proteins/metabolism |
| مستخلص: | 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 accelerated in growth due to cyclin D1 upregulation, and nuclear VP40 was found bound to the cyclin D1 promoter. Accelerated cell cycling was related to EV biogenesis, resulting in fewer but larger EVs. VP40 EV contents were enriched in ribonucleic acid-binding proteins and cytokines (interleukin-15, transforming growth factor-β1, and interferon-γ). Finally, EBOV-infected cell and animal EVs contained VP40, nucleoprotein, and glycoprotein. Conclusions: Nuclear VP40 upregulates cyclin D1 levels, resulting in dysregulated cell cycle and EV biogenesis. Packaging of cytokines and EBOV proteins into EVs from infected cells may be responsible for the decimation of immune cells during EBOV pathogenesis. |
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| معلومات مُعتمدة: | HHSN272200700016I United States AI NIAID NIH HHS; R01 AR068436 United States AR NIAMS NIH HHS; R01 NS099029 United States NS NINDS NIH HHS; R33 CA206937 United States CA NCI NIH HHS |
| المشرفين على المادة: | 0 (Glycoproteins) 0 (Nucleoproteins) 0 (Viral Core Proteins) 0 (Viral Matrix Proteins) 0 (nucleoprotein VP40, Ebola virus) 136601-57-5 (Cyclin D1) |
| تواريخ الأحداث: | Date Created: 20180901 Date Completed: 20190916 Latest Revision: 20240613 |
| رمز التحديث: | 20240613 |
| مُعرف محوري في PubMed: | PMC6249571 |
| DOI: | 10.1093/infdis/jiy472 |
| PMID: | 30169850 |
| قاعدة البيانات: | MEDLINE |
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