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. 2022 Nov 25;10:1053139. doi: 10.3389/fcell.2022.1053139

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Copyright © 2022 Turner and Mathias.

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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Inside the host cell nucleus, viral genomes circularise, and IE gene expression commences independently of viral protein synthesis. The MIEP is immediately upstream of the IE genes and acts as a hub for transcriptional activation or repression of the IE proteins by diverse host and viral factors. MIEP regulation also dictates the switch from lytic replication to latency and vice versa. The MIEP begins immediately upstream of the UL122/UL123 ORF and consists of the core (+1 to −40), enhancer (−40 to −550), unique (−550 to −750) and modulator (−750 to −1,140) regions. The IE1 and IE2 proteins are the main IE effectors which are encoded by the UL122/UL123 ORF by alternative splicing. IE1-72 and IE2-86 are multifunctional proteins that transactivate DE viral genes, remodel chromatin, disrupt interferon signalling, and inhibit apoptosis to create a conducive cellular environment for viral replication. IE, immediate early; MIEP, major immediate early promoter; ORF, open reading frame; DE, delayed early; crs, cis-repression sequence.