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. 2020 Sep 15;51:118. doi: 10.1186/s13567-020-00843-4

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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PRV UL13 inhibits poly(I:C)- or VSV-induced IFN-β transactivation. A, C PK15 cells were transfected with IFN-β-Luc (200 ng), pCMV-RL (2 ng) mixed with pcDNA3-Flag (200 ng), or pcDNA3-Flag-UL13 (200 ng) for 24 h; the cells were then treated with poly(I:C) (10 μg/mL) in (A) or infected with VSV (1 MOI) in (C) for 9 h. The fold activation of luciferase activity is the product of the luciferase activity induced by poly(I:C) with or without PRV UL13 divided by that induced by the empty vector. B, D The dual-luciferase reporter assays were performed as in (A, C), except that IRF3-Luc was used instead of IFN-β-Luc.