Abstract
Zika virus (ZIKV) is a mosquito-borne flavivirus that has emerged and caused global outbreaks since 2007. Although ZIKV proteins have been shown to suppress early anti-viral innate immune responses, little is known about the exact mechanisms. This study demonstrates that infection with either the African or Asian lineage of ZIKV leads to a modulated expression of suppressor of cytokine signaling (SOCS) genes encoding SOCS1 and SOCS3 in the following cell models: A549 human lung adenocarcinoma cells; JAr human choriocarcinoma cells; human neural progenitor cells. Studies of viral gene expression in response to SOCS1 or SOCS3 demonstrated that the knockdown of these SOCS proteins inhibited viral NS5 or ZIKV RNA expression, whereas overexpression resulted in an increased expression. Moreover, the overexpression of SOCS1 or SOCS3 inhibited the retinoic acid-inducible gene-I-like receptor-mediated activation of both type I and III interferon pathways. These results imply that SOCS upregulation following ZIKV infection modulates viral replication, possibly via the regulation of anti-viral innate immune responses.
Original language | English |
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Article number | 163 |
Journal | Pathogens |
Volume | 9 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2020 Mar |
Externally published | Yes |
Bibliographical note
Funding Information:Acknowledgments: This research was funded by the Basic Science Research Program of the National Research Foundation of Korea (NRF), by the Ministry of Science, ICT & Future Planning (NRF-2019R1A2C1005961).
Publisher Copyright:
© 2020 by the authors. Licensee MDPI, Basel, Switzerland.
Keywords
- Antiviral
- Interferon
- Suppressor of cytokine signaling
- Zika virus
ASJC Scopus subject areas
- Immunology and Allergy
- Molecular Biology
- General Immunology and Microbiology
- Microbiology (medical)
- Infectious Diseases