Coxsackievirus B3 Infection of Human Neural Progenitor Cells Results in Distinct Expression Patterns of Innate Immune Genes
- Authors
- Oh, Soo-Jin; Gim, Jeong-An; Lee, Jae Kyung; Park, Hosun; Shin, Ok Sarah
- Issue Date
- Mar-2020
- Publisher
- Multidisciplinary Digital Publishing Institute (MDPI)
- Keywords
- Coxsackievirus B3 (CVB3); gene expression profiles; neuronal progenitor cells; interferons; suppressor of cytokine signaling
- Citation
- Viruses, v.12, no.3
- Indexed
- SCIE
SCOPUS
- Journal Title
- Viruses
- Volume
- 12
- Number
- 3
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/987
- DOI
- 10.3390/v12030325
- ISSN
- 1999-4915
1999-4915
- Abstract
- Coxsackievirus B3 (CVB3), a member of Picornaviridae family, is an important human pathogen that causes a wide range of diseases, including myocarditis, pancreatitis, and meningitis. Although CVB3 has been well demonstrated to target murine neural progenitor cells (NPCs), gene expression profiles of CVB3-infected human NPCs (hNPCs) has not been fully explored. To characterize the molecular signatures and complexity of CVB3-mediated host cellular responses in hNPCs, we performed QuantSeq 3 ' mRNA sequencing. Increased expression levels of viral RNA sensors (RIG-I, MDA5) and interferon-stimulated genes, such as IFN-beta, IP-10, ISG15, OAS1, OAS2, Mx2, were detected in response to CVB3 infection, while IFN-gamma expression level was significantly downregulated in hNPCs. Consistent with the gene expression profile, CVB3 infection led to enhanced secretion of inflammatory cytokines and chemokines, such as interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1). Furthermore, we show that type I interferon (IFN) treatment in hNPCs leads to significant attenuation of CVB3 RNA copy numbers, whereas, type II IFN (IFN-gamma) treatment enhances CVB3 replication and upregulates suppressor of cytokine signaling 1/3 (SOCS) expression levels. Taken together, our results demonstrate the distinct molecular patterns of cellular responses to CVB3 infection in hNPCs and the pro-viral function of IFN-gamma via the modulation of SOCS expression.
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Collections - 3. Graduate School > Biomedical Research Center > 1. Journal Articles
- 5. Others > Medical Science Research Management Center > 1. Journal Articles
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