A spliced latency-associated VZV transcript maps antisense to the viral transactivator gene 61

Daniel P. Depledge, Werner J. D. Ouwendijk, Tomohiko Sadaoka, Shirley E. Braspenning, Yasuko Mori, Randall J. Cohrs, Georges M. G. M. Verjans () and Judith Breuer ()
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Daniel P. Depledge: University College London
Werner J. D. Ouwendijk: Erasmus Medical Centre
Tomohiko Sadaoka: Kobe University Graduate School of Medicine
Shirley E. Braspenning: Erasmus Medical Centre
Yasuko Mori: Kobe University Graduate School of Medicine
Randall J. Cohrs: University of Colorado School of Medicine
Georges M. G. M. Verjans: Erasmus Medical Centre
Judith Breuer: University College London

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract Varicella-zoster virus (VZV), an alphaherpesvirus, establishes lifelong latent infection in the neurons of >90% humans worldwide, reactivating in one-third to cause shingles, debilitating pain and stroke. How VZV maintains latency remains unclear. Here, using ultra-deep virus-enriched RNA sequencing of latently infected human trigeminal ganglia (TG), we demonstrate the consistent expression of a spliced VZV mRNA, antisense to VZV open reading frame 61 (ORF61). The spliced VZV latency-associated transcript (VLT) is expressed in human TG neurons and encodes a protein with late kinetics in productively infected cells in vitro and in shingles skin lesions. Whereas multiple alternatively spliced VLT isoforms (VLTly) are expressed during lytic infection, a single unique VLT isoform, which specifically suppresses ORF61 gene expression in co-transfected cells, predominates in latently VZV-infected human TG. The discovery of VLT links VZV with the other better characterized human and animal neurotropic alphaherpesviruses and provides insights into VZV latency.

Date: 2018
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DOI: 10.1038/s41467-018-03569-2

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