Journal
CELL DISCOVERY
Volume 3, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/celldisc.2017.6
Keywords
antiviral immunity; nonstructural proteins; type I interferon signaling; Zika virus
Categories
Funding
- National Key Basic Research Program of China [2015CB859800]
- National Natural Science Foundation of China [31522018, 31170832]
- Guangdong Natural Science Funds for Distinguished Young Scholar [S2013050014772]
- Fundamental Research Funds for the Central Universities [15lgjc02]
- Training Program for Outstanding Young Teachers in Higher Education institutions of Guangdong Province [YQ2015001]
- Guangzhou Science and Technology Project [201605030012]
- National Key Research Program of China [2016YFD0500300]
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Type I interferon (IFN) serves as the first line of defense against invading pathogens. Inhibition of IFN-triggered signaling cascade by Zika virus (ZIKV) plays a critical role for ZIKV to evade antiviral responses from host cells. Here we demonstrate that ZIKV nonstructural proteins NS1, NS4B and NS2B3 inhibit the induction of IFN and downstream IFN-stimulated genes through diverse strategies. NS1 and NS4B of ZIKV inhibit IFN beta signaling at TANK-binding kinase 1 level, whereas NS2B-NS3 of ZIKV impairs JAK-STAT signaling pathway by degrading Jak1 and reduces virus-induced apoptotic cell death. Furthermore, co-operation of NS1, NS4B and NS2B3 further enhances viral infection by blocking IFN-induced autophagic degradation of NS2B3. Hence, our study reveals a novel antagonistic system employing multiple ZIKV nonstructural proteins in restricting the innate antiviral responses.
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