ArticleJournal of virology2006
Bovine herpesvirus 1 UL49.5 protein inhibits the transporter associated with antigen processing despite complex formation with glycoprotein M.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 58 citations in OpenAlex.
- pUS6 in pseudorabies virus participates in the process of inhibiting antigen presentation by inhibiting the assembly of peptide loading complex.BMC veterinary research · 2024Article
- The herpesvirus UL49.5 protein hijacks a cellular C-degron pathway to drive TAP transporter degradation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Role of IFITM Proteins in Tick-Borne Encephalitis Virus Infection.Journal of virology · 2022Article
- The Roles of Envelope Glycoprotein M in the Life Cycle of Some Alphaherpesviruses.Frontiers in microbiology · 2021Review
- Palmitoylated mNeonGreen Protein as a Tool for Visualization and Uptake Studies of Extracellular Vesicles.Membranes · 2020Article
- Alphaherpesvirus gB Homologs Are Targeted to Extracellular Vesicles, but They Differentially Affect MHC Class II Molecules.Viruses · 2020Article
- Fluorescent TAP as a Platform for Virus-Induced Degradation of the Antigenic Peptide Transporter.Cells · 2019Article
- Structure determination of UL49.5 transmembrane protein from bovine herpesvirus 1 by NMR spectroscopy and molecular dynamics.Biochimica et biophysica acta. Biomembranes · 2019Article
- Bovine Herpesvirus 1 Counteracts Immune Responses and Immune-Surveillance to Enhance Pathogenesis and Virus Transmission.Frontiers in immunology · 2019Review
- Bovine Herpesvirus 1 UJournal of virology · 2018Article
- 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
- Molecular characterization of duck enteritis virus CHv strain UL49.5 protein and its colocalization with glycoprotein M.Journal of veterinary science · 2014Article
- Equine herpesvirus type 4 UL56 and UL49.5 proteins downregulate cell surface major histocompatibility complex class I expression independently of each other.Journal of virology · 2012Article
- The capacity of UL49.5 proteins to inhibit TAP is widely distributed among members of the genus Varicellovirus.Journal of virology · 2011Article
- Exploitation of herpesvirus immune evasion strategies to modify the immunogenicity of human mesenchymal stem cell transplants.PloS one · 2011Article
- Article
- Immune responses to Epstein-Barr virus: molecular interactions in the virus evasion of CD8+ T cell immunity.Microbes and infection · 2010Review
- Early, active, and specific localization of herpes simplex virus type 1 gM to nuclear membranes.Journal of virology · 2009Article
- Regulation of Innate Immune Responses by Bovine Herpesvirus 1 and Infected Cell Protein 0 (bICP0).Viruses · 2009Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bovine herpesvirus 1 (BHV-1) interferes with peptide translocation by the transporter associated with antigen processing (TAP). Recently, the UL49.5 gene product of BHV-1 was identified as the protein responsible for the observed inhibition of TAP. In BHV-1-infected cells and virions, the UL49.5 protein forms a complex with glycoprotein M (gM). Hence, it was investigated whether UL49.5 can combine the interactions with gM and the TAP complex. In cell lines constitutively expressing both UL49.5 and gM, UL49.5 appears to be required for functional processing of gM. Immunofluorescence-confocal laser scanning microscopy demonstrated that both proteins are interdependent for their redistribution from the endoplasmic reticulum to the trans-Golgi network. Remarkably, expression of cloned gM results in the abrogation of the UL49.5-mediated inhibition of TAP and prevents the degradation of the transporter. However, in BHV-1-infected cells, differences in UL49.5 and gM expression kinetics were seen to create a window of opportunity at the early stages of infection, during which time the UL49.5 protein can act on TAP without gM interference. Moreover, in later periods, non-gM-associated UL49.5 can be detected in addition to the UL49.5/gM complex. Thus, it has been deduced that different functions of UL49.5, editing of gM processing and inhibition of TAP, can be combined during BHV-1 infection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.