Impact of Zika virus on the human type I interferon osteoimmune response
| Autor: | Kamela Bellovoda, Marian Kalocsay, Arnaud Drouin, Dahlene N. Fusco, Scarlett Se Yun Cheon, Nicholas Wallbillich, Sharon Y. Liu, Matthew J. Berberich, Jason Zavras, Frederick Gootkind, Joshua Katz, Fernando P. S. Guastaldi, Maria J. Troulis, Nicolas Salvadori, Emily Bierman, Marc W. Theberge |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Proteomics Microcephaly Proteome Osteoimmunology Immunology Biology Virus Replication Biochemistry Antiviral Agents Zika virus 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Interferon Cell Line Tumor Chlorocebus aethiops medicine Immunology and Allergy Animals Humans Permissive Molecular Biology Vero Cells Mice Knockout Osteoblasts Zika Virus Infection Osteoblast Hematology Zika Virus medicine.disease biology.organism_classification Virology In vitro 030104 developmental biology medicine.anatomical_structure Gene Expression Regulation 030220 oncology & carcinogenesis Host-Pathogen Interactions Interferon Type I medicine.drug |
| Zdroj: | Cytokine. 137 |
| ISSN: | 1096-0023 |
| Popis: | Background The developing field of osteoimmunology supports importance of an interferon (IFN) response pathway in osteoblasts. Clarifying osteoblast-IFN interactions is important because IFN is used as salvage anti-tumor therapy but systemic toxicity is high with variable clinical results. In addition, osteoblast response to systemic bursts and disruptions of IFN pathways induced by viral infection may influence bone remodeling. ZIKA virus (ZIKV) infection impacts bone development in humans and IFN response in vitro. Consistently, initial evidence of permissivity to ZIKV has been reported in human osteoblasts. Hypothesis Osteoblast-like Saos-2 cells are permissive to ZIKV and responsive to IFN. Methods Multiple approaches were used to assess whether Saos-2 cells are permissive to ZIKV infection and exhibit IFN-mediated ZIKV suppression. Proteomic methods were used to evaluate impact of ZIKV and IFN on Saos-2 cells. Results Evidence is presented confirming Saos-2 cells are permissive to ZIKV and support IFN-mediated suppression of ZIKV. ZIKV and IFN differentially impact the Saos-2 proteome, exemplified by HELZ2 protein which is upregulated by IFN but non responsive to ZIKV. Both ZIKV and IFN suppress proteins associated with microcephaly/pseudo-TORCH syndrome (BI1, KI20A and UBP18), and ZIKV induces potential entry factor PLVAP. Conclusions Transient ZIKV infection influences osteoimmune state, and IFN and ZIKV activate distinct proteomes in Saos-2 cells, which could inform therapeutic, engineered, disruptions. |
| Databáze: | OpenAIRE |
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