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. 2019 Dec 21;12(1):17. doi: 10.3390/v12010017

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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HSV-1 inhibits the UPR and the ISR. HSV-1 infection causes translocation of ATF6 to the Golgi apparatus, where is it cleaved by S1P and S2P to yield the ATF6-N bZIP transcription factor. Despite this, ATF6-N responsive genes are not transcribed in HSV-1 infected cells. HSV-1 triggers IRE1 kinase activity, but represses XBP1 splicing and XBP1s synthesis, and subsequent XBP1s-dependent transcription. HSV-1 glycoprotein B (gB) binds to PERK and prevents its activation, thereby limiting eIF2α phosphorylation and maintaining bulk protein synthesis. HSV-1 γ34.5 protein acts similarly to GADD34, recruiting the cellular PP1 phosphatase to eIF2a and reinforcing the blockade on ISR activation. As a result, ATF4 is not synthesized and ATF4-responsive genes remain dormant.