Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.

Varicella zoster virus (VZV) is a human-specific herpesvirus that establishes latency in peripheral neurons. The only transcripts detected in infected human trigeminal ganglia (TG) obtained shortly after death correspond to the VZV latency-associated transcript (VLT) and associated VLT-ORF63 splice...

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Main Authors: Jiayi Wang, Nadine Brückner, Simon Weissmann, Thomas Günther, Shuyong Zhu, Carolin Vogt, Guorong Sun, Rongrong Guo, Renzo Bruno, Birgit Ritter, Lars Steinbrück, Benedikt B Kaufer, Daniel P Depledge, Adam Grundhoff, Abel Viejo-Borbolla
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2025-02-01
Series:PLoS Pathogens
Online Access:https://doi.org/10.1371/journal.ppat.1012367
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author Jiayi Wang
Nadine Brückner
Simon Weissmann
Thomas Günther
Shuyong Zhu
Carolin Vogt
Guorong Sun
Rongrong Guo
Renzo Bruno
Birgit Ritter
Lars Steinbrück
Benedikt B Kaufer
Daniel P Depledge
Adam Grundhoff
Abel Viejo-Borbolla
author_facet Jiayi Wang
Nadine Brückner
Simon Weissmann
Thomas Günther
Shuyong Zhu
Carolin Vogt
Guorong Sun
Rongrong Guo
Renzo Bruno
Birgit Ritter
Lars Steinbrück
Benedikt B Kaufer
Daniel P Depledge
Adam Grundhoff
Abel Viejo-Borbolla
author_sort Jiayi Wang
collection DOAJ
description Varicella zoster virus (VZV) is a human-specific herpesvirus that establishes latency in peripheral neurons. The only transcripts detected in infected human trigeminal ganglia (TG) obtained shortly after death correspond to the VZV latency-associated transcript (VLT) and associated VLT-ORF63 splice variants. In vitro studies showed that VLT-ORF63 is translated into a protein (pVLT-ORF63) that induces VZV transcription. The mechanisms that lead to this restricted gene expression and the transition to lytic replication remain unknown, partly due to the difficulty of working with human neurons. In this study, we addressed whether the neuroblastoma-derived cell line SH-SY5Y could serve as a model to investigate the mechanisms that lead to repression of VZV gene expression followed by reactivation. VZV productively infected differentiated SH-SY5Y (dSH-SY5Y) whereas incubation with acyclovir (ACV) inhibited virus replication and induced a progressive repression of the virus. Upon removal of ACV there was production of viral particles in a subset of cells, while others contained non-replicating VZV genomes and VLT-containing transcripts for at least 20 days post-infection (dpi). Exogenous expression of VLT-ORF63 induced productive infection, suggesting that the non-replicating and repressed genomes remained functional. Interestingly, histone deposition was undetectable at VZV genomes in quiescently infected dSH-SY5Y cells, pointing to a potential novel mechanism leading to VZV repression in this neuronal setting.
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spelling doaj-art-4ae89ea9e09745b091d9d1082e88e5512025-08-20T02:56:12ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742025-02-01212e101236710.1371/journal.ppat.1012367Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.Jiayi WangNadine BrücknerSimon WeissmannThomas GüntherShuyong ZhuCarolin VogtGuorong SunRongrong GuoRenzo BrunoBirgit RitterLars SteinbrückBenedikt B KauferDaniel P DepledgeAdam GrundhoffAbel Viejo-BorbollaVaricella zoster virus (VZV) is a human-specific herpesvirus that establishes latency in peripheral neurons. The only transcripts detected in infected human trigeminal ganglia (TG) obtained shortly after death correspond to the VZV latency-associated transcript (VLT) and associated VLT-ORF63 splice variants. In vitro studies showed that VLT-ORF63 is translated into a protein (pVLT-ORF63) that induces VZV transcription. The mechanisms that lead to this restricted gene expression and the transition to lytic replication remain unknown, partly due to the difficulty of working with human neurons. In this study, we addressed whether the neuroblastoma-derived cell line SH-SY5Y could serve as a model to investigate the mechanisms that lead to repression of VZV gene expression followed by reactivation. VZV productively infected differentiated SH-SY5Y (dSH-SY5Y) whereas incubation with acyclovir (ACV) inhibited virus replication and induced a progressive repression of the virus. Upon removal of ACV there was production of viral particles in a subset of cells, while others contained non-replicating VZV genomes and VLT-containing transcripts for at least 20 days post-infection (dpi). Exogenous expression of VLT-ORF63 induced productive infection, suggesting that the non-replicating and repressed genomes remained functional. Interestingly, histone deposition was undetectable at VZV genomes in quiescently infected dSH-SY5Y cells, pointing to a potential novel mechanism leading to VZV repression in this neuronal setting.https://doi.org/10.1371/journal.ppat.1012367
spellingShingle Jiayi Wang
Nadine Brückner
Simon Weissmann
Thomas Günther
Shuyong Zhu
Carolin Vogt
Guorong Sun
Rongrong Guo
Renzo Bruno
Birgit Ritter
Lars Steinbrück
Benedikt B Kaufer
Daniel P Depledge
Adam Grundhoff
Abel Viejo-Borbolla
Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.
PLoS Pathogens
title Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.
title_full Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.
title_fullStr Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.
title_full_unstemmed Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.
title_short Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.
title_sort repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition
url https://doi.org/10.1371/journal.ppat.1012367
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