Characterization and mapping of equine herpesvirus type 1 immediate early, early, and late transcripts

Gray, Wayne L.; Baumann, Raymond P.; Robertson, Alice; O’Callaghan, Dennis J.; Staczek, John

doi:10.1016/0168-1702(87)90018-9

Cited by 73 publications

(71 citation statements)

References 17 publications

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“…The transcriptional pattern of the genome of EHV-1 is similar to that of HSV-1 (Cohen et al, 1975;Gray et al,, 1987;Honess & Roizman, 1974;Clements et al, 1977); therefore in comparison with two HSV-1 genes, an immediate early gene (IE1) and an early gene (UL42), we conclude that gene 67 polypeptide is in the early class. Labelling experiments have demonstrated that the protein is a phosphoprotein, but not a glycoprotein.…”

Section: Discussionmentioning

confidence: 98%

Identification and characterization of the protein product of gene 67 in equine herpesvirus type 1 strain Ab4

Sun

Maclean

Brown

1995

Journal of General Virology

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Section: Discussionmentioning

confidence: 98%

Identification and characterization of the protein product of gene 67 in equine herpesvirus type 1 strain Ab4

Sun

Maclean

Brown

1995

Journal of General Virology

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“…and is classified as an early protein; and VZV gE, previously assumed to be a late gene product (Montalvo et al, 1985;reviewed by Grose 1990) is most likely leaky-late due to its accumulation prior to virus DNA replication (Reichelt et al, 2009). The multiple immediate-early genes identified in HSV-1, VZV and bovine herpesvirus type 1 (BHV-1), an alphaherpesvirus of cattle (van Santen, 1991), contrast with the single immediate-early protein identified in the alphaherpesviruses, pseudorabies virus (Everett & Dunlop, 1984) and equine herpesvirus type 1 (Gray et al, 1987;Caughman et al, 1988). Nonetheless, all alphaherpesviruses encode an ICP4 equivalent whose major function is to initiate transcription from the virus genome and for VZV this is the only gene with TAATGARAT elements (Abmayr et al, 1985;Smith et al, 1992;Fraefel et al, 1994).…”

Section: Fate Of Incoming Dnamentioning

confidence: 99%

A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation

Kennedy

Rovnak

Badani

et al. 2015

Journal of General Virology

128

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Herpes simplex virus type 1 (HSV-1; human herpesvirus 1) and varicella-zoster virus (VZV; human herpesvirus 3) are human neurotropic alphaherpesviruses that cause lifelong infections in ganglia. Following primary infection and establishment of latency, HSV-1 reactivation typically results in herpes labialis (cold sores), but can occur frequently elsewhere on the body at the site of primary infection (e.g. whitlow), particularly at the genitals. Rarely, HSV-1 reactivation can cause encephalitis; however, a third of the cases of HSV-1 encephalitis are associated with HSV-1 primary infection. Primary VZV infection causes varicella (chickenpox) following which latent virus may reactivate decades later to produce herpes zoster (shingles), as well as an increasingly recognized number of subacute, acute and chronic neurological conditions. Following primary infection, both viruses establish a latent infection in neuronal cells in human peripheral ganglia. However, the detailed mechanisms of viral latency and reactivation have yet to be unravelled. In both cases latent viral DNA exists in an 'end-less' state where the ends of the virus genome are joined to form structures consistent with unit length episomes and concatemers, from which viral gene transcription is restricted. In latently infected ganglia, the most abundantly detected HSV-1 RNAs are the spliced products originating from the primary latency associated transcript (LAT). This primary LAT is an 8.3 kb unstable transcript from which two stable (1.5 and 2.0 kb) introns are spliced. Transcripts mapping to 12 VZV genes have been detected in human ganglia removed at autopsy; however, it is difficult to ascribe these as transcripts present during latent infection as early-stage virus reactivation may have transpired in the post-mortem time period in the ganglia. Nonetheless, low-level transcription of VZV ORF63 has been repeatedly detected in multiple ganglia removed as close to death as possible. There is increasing evidence that HSV-1 and VZV latency is epigenetically regulated. In vitro models that permit pathway analysis and identification of both epigenetic modulations and global transcriptional mechanisms of HSV-1 and VZV latency hold much promise for our future understanding in this complex area. This review summarizes the molecular biology of HSV-1 and VZV latency and reactivation, and also presents future directions for study. Received 5 January 2015Accepted 18 March 2015 IntroductionHerpes simplex virus type 1 (HSV-1; human herpesvirus 1) and varicella-zoster virus (VZV; human herpesvirus 3) are human neurotropic alphaherpesviruses usually acquired early in life. Primary HSV-1 infection is usually localized and may be asymptomatic, although it can produce a more widespread systemic infection in neonates and immunocompromised adults, whilst primary VZV infection is systemic and results in childhood varicella (chickenpox). During primary infection, both viruses gain access to neurons most likely through retrograde transport from the site of cutaneous lesion...

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“…It is proposed that the larger 4-6 kb transcript encodes the EHV-1 ICP 18.5, with the 5' region of each mRNA encoding the unique polypeptide. These two transcripts are probably equivalent to the 3.6 and 4-4 kb transcripts identified by Gray et al (1987) as coming from a similar region of the genome of EHV-1 (Kentucky A strain). No obvious poly(A) signal is evident downstream from the EHV-1 ICP 18.50RF, whereas a polyadenylation signal occurs a few nucleotides from the termination codon of the EHV-1 gB ORF, suggesting that the two transcripts have a common 3' terminus.…”

Section: Virus Neutralization Testmentioning

confidence: 99%

Transcript Analysis of The Equine Herpesvirus 1 Glycoprotein B Gene Homologue and Its Expression by a Recombinant Vaccinia Virus

Bell

Boyle

Whalley

1990

Journal of General Virology

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Characterization and mapping of equine herpesvirus type 1 immediate early, early, and late transcripts

Cited by 73 publications

References 17 publications

Identification and characterization of the protein product of gene 67 in equine herpesvirus type 1 strain Ab4

Identification and characterization of the protein product of gene 67 in equine herpesvirus type 1 strain Ab4

A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation

Transcript Analysis of The Equine Herpesvirus 1 Glycoprotein B Gene Homologue and Its Expression by a Recombinant Vaccinia Virus

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