Varicella-zoster virus (VZV) transcription during latency in human ganglia: prevalence of VZV gene 21 transcripts in latently infected human ganglia

Cohrs, Randall J.; Barbour, M B; Mahalingam, Ravi; Wellish, Mary; Gilden, Donald H.

doi:10.1128/jvi.69.4.2674-2678.1995

Cited by 58 publications

(15 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ganglia were pooled in a prechilled motor and powdered under liquid nitrogen. From the 16.5 g of powdered ganglia, ϳ0.3 g was removed for DNA extraction, and total RNA was extracted from the remaining tissue (2,3). Poly(A) ϩ RNA was selected from total RNA by chromatography on oligo(dT) spin columns as directed by Clontech (Palo Alto, Calif.).…”

Section: Methodsmentioning

confidence: 99%

“…Table 2 lists the DNA sequence of the oligonucleotide primers used for PCR and the location of the VZV-specific oligonucleotide primers and orientation relative to the direction of gene transcription. PCR was conducted as described previously (2) except that cycling times were reduced to 30 s at 94ЊC, 30 s at 55ЊC, and 60 s at 72ЊC for a total of 35 cycles.…”

Section: Methodsmentioning

confidence: 99%

“…To further our understanding of VZV gene transcription during latency, we constructed a cDNA library from latently infected human trigeminal ganglionic poly(A) ϩ RNA enriched for VZV transcripts by hybridization to biotinylated VZV DNA. DNA extracted from the cDNA library was analyzed for the presence of transcripts from VZV genes, including genes 4, 61, 62, and 63, which encode immediate-early and regulatory proteins (7,9,12,23); gene 10, encoding a virion-associated transactivator (22); gene 51, encoding a protein that binds to the VZV origin of replication (31); gene 40, which encodes the major viral capsid protein (5); and genes 21, 29, and 62, which have been reported to be transcribed during latency (2,3,21).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Varicella-zoster virus (VZV) transcription during latency in human ganglia: detection of transcripts mapping to genes 21, 29, 62, and 63 in a cDNA library enriched for VZV RNA

Cohrs

Barbour

Gilden

1996

J Virol

Self Cite

162

View full text Add to dashboard Cite

Information on the extent of virus DNA transcription and translation in infected tissue is crucial to an understanding of herpesvirus latency. To detect low-abundance latent varicella-zoster virus (VZV) transcripts, poly(A) ؉ RNA extracted from latently infected human trigeminal ganglia was enriched for VZV transcripts by hybridization to biotinylated VZV DNA. After hybridization, the RNA-DNA hybrid was isolated by binding to avidin-coated beads and extensively washed, and the RNA was released by heat denaturation. A lambda-based cDNA library was then constructed from the enriched RNA. PCR and DNA sequencing of DNA extracted from the cDNA library revealed the presence of VZV genes 21, 29, 62, and 63, but not VZV genes 4, 10, 40, 51, and 61, in the enriched cDNA library. These findings confirm the detection of VZV gene 29 and 62 transcripts on Northern (RNA) blots prepared from latently infected human ganglia (J.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Varicella-zoster virus (VZV) transcription during latency in human ganglia: detection of transcripts mapping to genes 21, 29, 62, and 63 in a cDNA library enriched for VZV RNA

Cohrs

Barbour

Gilden

1996

J Virol

Self Cite

162

View full text Add to dashboard Cite

show abstract

“…In contrast to the restricted expression of the LATs marking HSV latency, which will be covered in detail in following sections, no corresponding transcription unit has been identified in the VZV genome, and no latencyspecific genes have been described. Instead, based upon analysis of neurons obtained at autopsy and with the proviso that traumatic reactivation in such material can never be rigorously excluded, VZV latency appears to involve the sporadic and low-level expression of one or another productive-phase viral transcripts, although there is some controversy about whether this gene expression takes place in sensory nerve ganglia, satellite cells, or both (36,37,48).…”

Section: Different Pattern Of Infection Latency and Reactivation-vamentioning

confidence: 99%

Experimental investigation of herpes simplex virus latency

1997

View full text Add to dashboard Cite

The clinical manifestations of herpes simplex virus infection generally involve a mild and localized primary infection followed by asymptomatic (latent) infection interrupted sporadically by periods of recrudescence (reactivation) where virus replication and associated cytopathologic findings are manifest at the site of initial infection. During the latent phase of infection, viral genomes, but not infectious virus itself, can be detected in sensory and autonomic neurons. The process of latent infection and reactivation has been subject to continuing investigation in animal models and, more recently, in cultured cells. The initiation and maintenance of latent infection in neurons are apparently passive phenomena in that no virus gene products need be expressed or are required. Despite this, a single latency-associated transcript (LAT) encoded by DNA encompassing about 6% of the viral genome is expressed during latent infection in a minority of neurons containing viral DNA. This transcript is spliced, and the intron derived from this splicing is stably maintained in the nucleus of neurons expressing it. Reactivation, which can be induced by stress and assayed in several animal models, is facilitated by the expression of LAT. Although the mechanism of action of LAT-mediated facilitation of reactivation is not clear, all available evidence argues against its involving the expression of a protein. Rather, the most consistent models of action involve LAT expression playing a cis-acting role in a very early stage of the reactivation process.

show abstract

“…Ganglion cells within which VZV is latent, can survive for years. Only a limited set of viral genes is transcribed during latency; these encode immediate early and early proteins (ORF4,21,29,62,63,40,66) but gps are not expressed (Cohrs et al 1995Croen et al 1988;Gershon et al 2008b;Kennedy et al 2000Kennedy et al , 2001Lungu et al 1998). Neurons in which VZV reactivates display lytic infection.…”

Section: Introductionmentioning

confidence: 99%

VZV Infection of Keratinocytes: Production of Cell-Free Infectious Virions In Vivo

Gershon

2010

Current Topics in Microbiology and Immunology

View full text Add to dashboard Cite

Varicella-zoster virus (VZV) is the cause of varicella (chickenpox) and zoster (shingles). Varicella is a primary infection that spreads rapidly in epidemics while zoster is a secondary infection that occurs sporadically as a result of the reactivation of previously acquired VZV. Reactivation is made possible by the establishment of latency during the initial episode of varicella. The signature lesions of both varicella and zoster are cutaneous vesicles, which are filled with a clear fluid that is rich in infectious viral particles. It has been postulated that the skin is the critical organ in which both host-to-host transmission of VZV and the infection of neurons to establish latency occur. This hypothesis is built on evidence that the large cation-independent mannose 6-phosphate receptor (MPRci) interacts with VZV in virtually all infected cells, except those of the suprabasal epidermis, in a way that prevents the release of infectious viral particles. Specifically, the virus is diverted in an MPRci-dependent manner from the secretory pathway to late endosomes where VZV is degraded. Because nonepidermal cells are thus prevented from releasing infectious VZV, a slow process, possibly involving fusion of infected cells with their neighbors, becomes the means by which VZV is disseminated. In the epidermis, however, the maturation of keratinocytes to give rise to corneocytes in the suprabasal epidermis is associated uniquely with a downregulation of the MPRci. As a result, the diversion of VZV to late endosomes does not occur in the suprabasal epidermis where vesicular lesions occur. The formation of the waterproof, chemically resistant barrier of the epidermis, however, requires that constitutive secretion outlast the downregulation of the endosomal pathway. Infectious VZV is therefore secreted by default, accounting for the presence of infectious virions in vesicular fluid. Sloughing of corneocytes, aided by scratching, then aerosolizes the virus, which can float with dust to be inhaled by susceptible hosts. Infectious virions also bathe the terminals of those sensory neurons that innervate the epidermis. These terminals become infected with VZV and provide a route, retrograde transport, which can conduct VZV to cranial nerve (CNG), dorsal root ganglia (DRG), and enteric ganglia (EG) to establish latency. Reactivation returns VZV to the skin, now via anterograde transport in axons, to cause the lesions of zoster. Evidence in support of these hypotheses includes observations of the VZV-infected human epidermis and studies of guinea pig neurons in an in vitro model system.

show abstract

Varicella-zoster virus (VZV) transcription during latency in human ganglia: prevalence of VZV gene 21 transcripts in latently infected human ganglia

Cited by 58 publications

References 26 publications

Varicella-zoster virus (VZV) transcription during latency in human ganglia: detection of transcripts mapping to genes 21, 29, 62, and 63 in a cDNA library enriched for VZV RNA

Varicella-zoster virus (VZV) transcription during latency in human ganglia: detection of transcripts mapping to genes 21, 29, 62, and 63 in a cDNA library enriched for VZV RNA

Experimental investigation of herpes simplex virus latency

VZV Infection of Keratinocytes: Production of Cell-Free Infectious Virions In Vivo

Contact Info

Product

Resources

About