ArticleJournal of virology2008
Simultaneous tracking of capsid, tegument, and envelope protein localization in living cells infected with triply fluorescent herpes simplex virus 1.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed.
- Impact of the changes in substrate specificity of herpes simplex virus 1 protein kinase Us3 on viral infectionJournal of virology · 2025Article
- Structural host-virus interactome profiling of intact infected cells.Nature communications · 2025Article
- The functions of herpesvirus shuttling proteins in the virus lifecycle.Frontiers in microbiology · 2025Review
- The loss of both pUL16 and pUL21 in HSV-1 infected cells abolishes cytoplasmic envelopment.bioRxiv : the preprint server for biology · 2024Article
- Impaired endocytosis and accumulation in early endosomal compartments defines herpes simplex virus-mediated disruption of the nonclassical MHC class I-related molecule MR1.The Journal of biological chemistry · 2024Article
- The Rab6 post-Golgi secretory pathway contributes to herpes simplex virus 1 (HSV-1) egress.Journal of virology · 2024Article
- Impact of the interaction between herpes simplex virus 1 ICP22 and FACT on viral gene expression and pathogenesis.Journal of virology · 2024Article
- Identification of a novel neurovirulence factor encoded by the cryptic orphan gene UL31.6 of herpes simplex virus 1.Journal of virology · 2024Article
- Pseudorabies virus hijacks the Rab6 protein to promote viral assembly and egress.Veterinary research · 2024Article
- A dual fluorescent herpes simplex virus type 1 recombinant reveals divergent outcomes of neuronal infection.Journal of virology · 2024Article
- Current Insights into the Maturation of Epstein-Barr Virus Particles.Microorganisms · 2024Review
- Major Virion Tegument Protein VP22 Targets Nuclear Matrix and Chromatin upon Entry into Cells during Productive Herpes Simplex Virus 1 Infection.Microorganisms · 2024Article
- Individual herpes simplex virus 1 (HSV-1) particles exit by exocytosis and accumulate at preferential egress sites.Journal of virology · 2024Article
- BGLF4 kinase regulates the formation of the EBV cytoplasmic assembly compartment and the recruitment of cellular IQGAP1 for virion release.Journal of virology · 2024Article
- Herpes Simplex Virus 1 (HSV-1) Uses the Rab6 Post-Golgi Secretory Pathway For Viral Egress.bioRxiv : the preprint server for biology · 2023Article
- GARP and EARP are required for efficient BoHV-1 replication as identified by a genome wide CRISPR knockout screen.PLoS pathogens · 2023Article
- Article
- LIVE-CELL FLUORESCENCE MICROSCOPY OF HSV-1 CELLULAR EGRESS BY EXOCYTOSIS.bioRxiv : the preprint server for biology · 2023Article
- Mechanism of herpesvirus UL24 protein regulating viral immune escape and virulence.Frontiers in microbiology · 2023Review
- Redundant and Specific Roles of A-Type Lamins and Lamin B Receptor in Herpes Simplex Virus 1 Infection.Journal of virology · 2022Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We report here the construction of a triply fluorescent-tagged herpes simplex virus 1 (HSV-1) expressing capsid protein VP26, tegument protein VP22, and envelope protein gB as fusion proteins with monomeric yellow, red, and cyan fluorescent proteins, respectively. The recombinant virus enabled us to monitor the dynamics of these capsid, tegument, and envelope proteins simultaneously in the same live HSV-1-infected cells and to visualize single extracellular virions with three different fluorescent emissions. In Vero cells infected by the triply fluorescent virus, multiple cytoplasmic compartments were found to be induced close to the basal surfaces of the infected cells (the adhesion surfaces of the infected cells on the solid growth substrate). Major capsid, tegument, and envelope proteins accumulated and colocalized in the compartments, as did marker proteins for the trans-Golgi network (TGN) which has been implicated to be the site of HSV-1 secondary envelopment. Moreover, formation of the compartments was correlated with the dynamic redistribution of the TGN proteins induced by HSV-1 infection. These results suggest that HSV-1 infection causes redistribution of TGN membranes to form multiple cytoplasmic compartments, possibly for optimal secondary envelopment. This is the first real evidence for the assembly of all three types of herpesvirus proteins-capsid, tegument, and envelope membrane proteins-in TGN.
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