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. 2019 May 7;10:1008. doi: 10.3389/fimmu.2019.01008

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Copyright © 2019 Jones.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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BoHV-1 encoded immune-evasion genes that promote productive infection. Cellular mechanisms leading to innate immune antiviral signaling pathways are denoted in blue. Red lettering denotes viral genes that counteract antiviral signaling pathways. It is well-established that two protein kinases (IKK-ε +TBK1) activate the transcription factors (IRF3 and IRF7), which are required for activating the IFN-β promoter (96–98). The JNK protein kinase (c-Jun N-terminal kinases) activates the AP1 (activating protein 1) and ATF2 (activating transcription factor 2), which are also required for activating the IFN-β promoter (96–98). For further details, see the text.