ArticleJournal of virology2002
The gene 10 (UL49.5) product of equine herpesvirus 1 is necessary and sufficient for functional processing of glycoprotein M.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Bovine Herpesvirus 1 UJournal of virology · 2018Article
- Equine Herpesvirus 1 Multiply Inserted Transmembrane Protein pUL43 Cooperates with pUL56 in Downregulation of Cell Surface Major Histocompatibility Complex Class I.Journal of virology · 2015Article
- Viral inhibition of the transporter associated with antigen processing (TAP): a striking example of functional convergent evolution.PLoS pathogens · 2015Review
- Herpes simplex virus 1 gN partners with gM to modulate the viral fusion machinery.Journal of virology · 2015Article
- Characterization of glycoproteins in equine herpesvirus-1.The Journal of veterinary medical science · 2013Article
- Marek's disease virus expresses multiple UL44 (gC) variants through mRNA splicing that are all required for efficient horizontal transmission.Journal of virology · 2012Article
- Identification and characterization of equine herpesvirus type 1 pUL56 and its role in virus-induced downregulation of major histocompatibility complex class I.Journal of virology · 2012Article
- Article
- Early, active, and specific localization of herpes simplex virus type 1 gM to nuclear membranes.Journal of virology · 2009Article
- HCMV-encoded glycoprotein M (UL100) interacts with Rab11 effector protein FIP4.Traffic (Copenhagen, Denmark) · 2009Article
- Varicellovirus UL 49.5 proteins differentially affect the function of the transporter associated with antigen processing, TAP.PLoS pathogens · 2008Article
- The cytoplasmic tail of glycoprotein M (gpUL100) expresses trafficking signals required for human cytomegalovirus assembly and replication.Journal of virology · 2007Article
- The carboxy-terminal domain of glycoprotein N of human cytomegalovirus is required for virion morphogenesis.Journal of virology · 2007Article
- Glycoprotein M of herpes simplex virus 1 is incorporated into virions during budding at the inner nuclear membrane.Journal of virology · 2007Article
- Bovine herpesvirus 1 UL49.5 protein inhibits the transporter associated with antigen processing despite complex formation with glycoprotein M.Journal of virology · 2006Article
- Human cytomegalovirus infection elicits a glycoprotein M (gM)/gN-specific virus-neutralizing antibody response.Journal of virology · 2006Article
- The alpha-TIF (VP16) homologue (ETIF) of equine herpesvirus 1 is essential for secondary envelopment and virus egress.Journal of virology · 2006Article
- The equine herpesvirus 1 UL20 product interacts with glycoprotein K and promotes egress of mature particles.Journal of virology · 2006Article
- High-level expression of Marek's disease virus glycoprotein C is detrimental to virus growth in vitro.Journal of virology · 2005Article
- Varicelloviruses avoid T cell recognition by UL49.5-mediated inactivation of the transporter associated with antigen processing.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
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4 authors.
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Abstract
The functional cooperation of equine herpesvirus 1 (EHV-1) glycoprotein M (gM) and the gene 10 (UL49.5) product was analyzed. Transient-transfection experiments using gM and UL49.5 expression plasmids as well as RK13 cell lines constitutively expressing UL49.5 (RK49.5) or gM (RKgM) demonstrated that the endo-beta-N-acetylglucosaminidase H (endo H)-resistant mature form of gM was detectable only after coexpression of the two proteins. Deletion of the EHV-1 UL49.5-homologous gene 10 in strain KyA resulted in a small-plaque phenotype and up to 190-fold-reduced virus titers. The growth defects of the mutant KyA Delta 49.5 virus, which were very similar to those of a gM-negative KyA virus, could be completely compensated for by growth of the mutant virus on RK49.5 cells or by repairing the deletion of gene 10 in the revertant virus KyA Delta 49.5R. Analysis of cells infected with the UL49.5-negative EHV-1 demonstrated that gM was not transported to the trans-Golgi network in the absence of the UL49.5 product. In contrast, gM was efficiently transported and processed to the endo H-resistant mature form in KyA Delta 49.5-infected RK49.5 cells. Furthermore, radioimmunoprecipitation experiments demonstrated that gM maturation was observed only if a 10,000-M(r) protein was coprecipitated with gM in KyA- or KyA Delta 49.5R-infected cells or virions. This protein was absent in cells infected with Ky Delta 49.5 or KyA Delta gM, suggesting that it was the EHV-1 UL49.5 product. Taken together, our results demonstrate that the expression of the EHV-1 UL49.5 product is necessary and sufficient for gM processing and that it is required for efficient virus replication.
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