Widespread activation of antisense transcription of the host genome during herpes simplex virus 1 infection

Please always quote using this URN: urn:nbn:de:bvb:20-opus-173381
  • Background Herpesviruses can infect a wide range of animal species. Herpes simplex virus 1 (HSV-1) is one of the eight herpesviruses that can infect humans and is prevalent worldwide. Herpesviruses have evolved multiple ways to adapt the infected cells to their needs, but knowledge about these transcriptional and post-transcriptional modifications is sparse. Results Here, we show that HSV-1 induces the expression of about 1000 antisense transcripts from the human host cell genome. A subset of these is also activated by the closely relatedBackground Herpesviruses can infect a wide range of animal species. Herpes simplex virus 1 (HSV-1) is one of the eight herpesviruses that can infect humans and is prevalent worldwide. Herpesviruses have evolved multiple ways to adapt the infected cells to their needs, but knowledge about these transcriptional and post-transcriptional modifications is sparse. Results Here, we show that HSV-1 induces the expression of about 1000 antisense transcripts from the human host cell genome. A subset of these is also activated by the closely related varicella zoster virus. Antisense transcripts originate either at gene promoters or within the gene body, and they show different susceptibility to the inhibition of early and immediate early viral gene expression. Overexpression of the major viral transcription factor ICP4 is sufficient to turn on a subset of antisense transcripts. Histone marks around transcription start sites of HSV-1-induced and constitutively transcribed antisense transcripts are highly similar, indicating that the genetic loci are already poised to transcribe these novel RNAs. Furthermore, an antisense transcript overlapping with the BBC3 gene (also known as PUMA) transcriptionally silences this potent inducer of apoptosis in cis. Conclusions We show for the first time that a virus induces widespread antisense transcription of the host cell genome. We provide evidence that HSV-1 uses this to downregulate a strong inducer of apoptosis. Our findings open new perspectives on global and specific alterations of host cell transcription by viruses.show moreshow less

Download full text files

Export metadata

Additional Services

Share in Twitter Search Google Scholar Statistics
Metadaten
Author: Emanuel Wyler, Jennifer Menegatti, Vedran Franke, Christine Kocks, Anastasiya Boltengagen, Thomas Hennig, Kathrin Theil, Andrzej Rutkowski, Carmelo Ferrai, Laura Baer, Lisa Kermas, Caroline Friedel, Nikolaus Rajewsky, Altuna Akalin, Lars Dölken, Friedrich Grässer, Markus Landthaler
URN:urn:nbn:de:bvb:20-opus-173381
Document Type:Journal article
Faculties:Medizinische Fakultät / Institut für Virologie und Immunbiologie
Language:English
Parent Title (English):Genome Biology
Year of Completion:2017
Volume:18
Article Number:209
Source:Genome Biology (2017) 18:209.https://doi.org/10.1186/s13059-017-1329-5
DOI:https://doi.org/10.1186/s13059-017-1329-5
Pubmed Id:https://pubmed.ncbi.nlm.nih.gov/29089033
Dewey Decimal Classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Tag:Antisense; BBC3; Herpes; ICP4; IncRNA; NFKB; Transcription; Virology; Virus
Release Date:2021/11/02
Licence (German):License LogoCC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International