Varicella-Zoster Virus Retains Major Histocompatibility Complex Class I Proteins in the Golgi Compartment of Infected Cells

Abendroth, Allison; Lin, I Winnie; Slobedman, Barry; Ploegh, Hidde L.; Arvin, Ann M.

doi:10.1128/jvi.75.10.4878-4888.2001

Cited by 121 publications

(98 citation statements)

References 50 publications

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“…The varicella zoster virus-encoded UL49.5 protein did not block peptide transport (Fig. 12), which is in agreement with earlier findings in infected cells (31).…”

Section: Ul495 Arrests Tap In a Translocation-incompetent Statesupporting

confidence: 82%

“…Various members of the varicellovirus group down-modulate MHC class I expression (29)(30)(31)(32)(33)(34). Among these viruses, bovine herpesvirus 1 (BHV1), pseudorabies virus (PRV), and equine herpesvirus 1 (EHV1) abolish peptide transport by TAP, resulting in down-regulation of MHC class I surface expression.…”

Section: Detection and Elimination Of Virus-infected Cells By Cytotoxmentioning

confidence: 99%

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Varicelloviruses avoid T cell recognition by UL49.5-mediated inactivation of the transporter associated with antigen processing

Koppers-Lalić

Reits

Ressing

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

171

246

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“…The varicella zoster virus-encoded UL49.5 protein did not block peptide transport (Fig. 12), which is in agreement with earlier findings in infected cells (31).…”

Section: Ul495 Arrests Tap In a Translocation-incompetent Statesupporting

confidence: 82%

Section: Detection and Elimination Of Virus-infected Cells By Cytotoxmentioning

confidence: 99%

Varicelloviruses avoid T cell recognition by UL49.5-mediated inactivation of the transporter associated with antigen processing

Koppers-Lalić

Reits

Ressing

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

171

246

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Section: Fate Of Incoming Dnamentioning

confidence: 99%

“…In summary, HSV-1 immediate-early proteins efficiently inactivate host antivirus defence, commandeer the transcription apparatus and establish an environment conducive to continued virus gene expression. VZV also downregulates cell surface expression of MHC class I, but the accumulation of MHC class I molecules in Golgi compartments is attributed to the virus protein kinase encoded by VZV ORF66 (Abendroth et al, 2001; Eisfeld et al, 2007;Verweij et al, 2011).When sufficient immediate-early proteins accumulate, a switch in promoter usage takes place and early virus genes are transcribed. The 11 HSV-1 early genes encode enzymes that replicate virus DNA in two stages: first by h replication (Severini et al, 1994) followed by a s (rolling circle) mechanism (Skaliter et al, 1996).…”

mentioning

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

137

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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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“…The various mechanisms by which herpesviruses downregulate class I target virtually all stages of the class I expression pathway, including synthesis (Hirata et al, 2001), peptide transport (Ahn et al, 1997;Ambagala et al, 2000;Hill et al, 1995;Hinkley et al, 1998;Jugovic et al, 1998;Zeidler et al, 1997), transit to (Abendroth et al, 2001;Ahn et al, 1996;Campbell & Slater, 1994;del Val et al, 1992;Hudson et al, 2001;Jones & Sun, 1997;Jones et al, 1996;Reusch et al, 1999;Wiertz et al, 1996) and stability on the cell surface (Ishido et al, 2000). Although our data do not directly address mechanisms for class I down-regulation by GPCMV, our observation that the kinetics of class I loss in response to virus infection closely parallels the response to cycloheximide is consistent with a block to repopulation of surface class I; however, as multiple GPCMV genes may be involved, a detailed understanding of their mechanisms awaits identification of the viral genes and independent analyses of their effects.…”

mentioning

confidence: 99%

Down-regulation of surface major histocompatibility complex class I by guinea pig cytomegalovirus

Lacayo

Sato

Kamiya

et al. 2003

Journal of General Virology

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Varicella-Zoster Virus Retains Major Histocompatibility Complex Class I Proteins in the Golgi Compartment of Infected Cells

Cited by 121 publications

References 50 publications

Varicelloviruses avoid T cell recognition by UL49.5-mediated inactivation of the transporter associated with antigen processing

Varicelloviruses avoid T cell recognition by UL49.5-mediated inactivation of the transporter associated with antigen processing

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

Down-regulation of surface major histocompatibility complex class I by guinea pig cytomegalovirus

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