#LONZA BLUESENSE SKIN#

#LONZA BLUESENSE SKIN#

VLT encodes a protein with late kinetics during lytic VZV infection in vitro and in zoster skin lesions. Here, we describe the discovery and functional characterization of a VZV latency transcript (VLT), that maps antisense to VZV ORF 61 (the VZV ICP0 homologue 9, 10), and which is consistently expressed in neurons of latently infected human trigeminal ganglia (TG). The exception is varicella-zoster virus (VZV), an О±HV which infects over 90% of adults and for which neither a canonical latency transcript 1, 6вЂ“ 8 nor a putative mechanism for repressing lytic transcription during latency have been identified. These latency transcripts, either directly or through encoded miRNAs or proteins, repress expression of the ICP0 orthologues 3вЂ“ 5. For most О±HVs, including the best-studied herpes simplex type 1 ( HSV-1), viral latency is characterized by expression of a single or restricted set of transcripts that map antisense to the open reading frame (ORF) homologous to the major HSV immediate early viral transactivator, ICP0 2. The discovery of VLT directly unifies the latent VZV transcription program with those of better-characterized О±HVs, removing longstanding barriers to understanding VZV latency and paving the way for research into the development of vaccines that do not establish latency or reactivate, and drugs that eradicate latent VZV.Дuring primary infection, neurotropic alphaherpesviruses (О±HVs) gain access to neurons in sensory and cranial ganglia establishing lifelong latent infection from which they can later reactivate to cause debilitating disease 1. Whereas multiple alternatively spliced VLT isoforms are expressed during lytic VZV infection, a single unique VLT isoform that specifically suppresses ORF61 gene expression predominates in latently VZV-infected human TG. Here, we describe the discovery and functional characterization of a VZV latency transcript (VLT), that maps antisense to VZV ORF 61 (the VZV ICP0 homologue 9,10), and which is consistently expressed in neurons of latently infected human trigeminal ganglia (TG). The exception is varicella-zoster virus (VZV), an О±HV which infects over 90% of adults and for which neither a canonical latency transcript 1,6вЂ“8 nor a putative mechanism for repressing lytic transcription during latency have been identified. These latency transcripts, either directly or through encoded miRNAs or proteins, repress expression of the ICP0 orthologues 3вЂ“5. During primary infection, neurotropic alphaherpesviruses (О±HVs) gain access to neurons in sensory and cranial ganglia establishing lifelong latent infection from which they can later reactivate to cause debilitating disease 1.

Lonza bluesense