Coxsackievirus B3 infection of human neural progenitor cells results in distinct expression patterns of innate immune genes

Soo Jin Oh, Jeong An Gim, Jae Kyung Lee, Hosun Park, Ok Sarah Shin

Research output: Contribution to journalArticle

1 Citation (Scopus)

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-β, IP-10, ISG15, OAS1, OAS2, Mx2, were detected in response to CVB3 infection, while IFN-γ 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-γ) 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-γ via the modulation of SOCS expression.

Original languageEnglish
Article number32
JournalViruses
Volume12
Issue number3
DOIs
Publication statusPublished - 2020 Jan 1

Keywords

  • Coxsackievirus B3 (CVB3), gene expression profiles
  • Interferons
  • Neuronal progenitor cells
  • Suppressor of cytokine signaling

ASJC Scopus subject areas

  • Infectious Diseases
  • Virology

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