Journal
VIROLOGY
Volume 489, Issue -, Pages 252-268Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2015.12.010
Keywords
CREB-binding protein; Porcine epidemic diarrhea virus; Coronavirus; Interferon regulation; CBP; Nsp1; Innate immune signaling
Categories
Funding
- Agriculture and Food Research Initiative (AFRI) Competitive Grant of the USDA-NIFA [2013-67015-21243]
- USDA HATCH
- Multistate Research Fund
- NIFA [2013-67015-21243, 577464] Funding Source: Federal RePORTER
Ask authors/readers for more resources
Type I interferons (IFN-alpha/beta) are the major components of the innate immune response of hosts, and in turn many viruses have evolved to modulate the host response during infection. We found that the IFN-beta production was significantly suppressed during PEDV infection in cells. To identify viral IFN antagonists and to study their suppressive function, viral coding sequences for the entire structural and nonstructural proteins were cloned and expressed. Of 16 PEDV nonstructural proteins (nsps), nsp1, nsp3, nsp7, nsp14, nsp15 and nsp16 were found to inhibit the IFN-beta and IRF3 promoter activities. The sole accessory protein ORF3, structure protein envelope (E), membrane (M), and nucleocapsid (N) protein were also shown to inhibit such activities. PEDV nspl did not interfere the IRF3 phosphorylation and nuclear translocation but interrupted the enhanceosome assembly of IRF3 and CREB-binding protein (CBP) by degrading CBP. A further study showed that the CBP degradation by nspl was proteasome-dependent. Our data demonstrate that PEDV modulates the host innate immune responses by degrading CBP and suppressing ISGs expression. (C) 2015 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available