ArticleJournal of virology2007
Equine herpesvirus 1 enters cells by two different pathways, and infection requires the activation of the cellular kinase ROCK1.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 75 citations in OpenAlex.
- Herpes simplex virus 1 envelope glycoprotein C shields glycoprotein D to protect virions from entry-blocking antibodies.Journal of virology · 2025Article
- Temporal transcriptional profiling of host cells infected by a veterinary alphaherpesvirus using nanopore sequencing.Scientific reports · 2025Article
- Virus infection and vesicle trafficking.Frontiers in immunology · 2025Review
- Herpes Simplex Virus 1 Envelope Glycoprotein C Shields Glycoprotein D to Protect Virions from Entry-Blocking Antibodies.bioRxiv : the preprint server for biology · 2024Article
- Oncolytic herpes simplex viruses designed for targeted treatment of EGFR-bearing tumors.Molecular therapy. Oncology · 2024Article
- RhoA suppresses pseudorabies virus replication in vitro.Virology journal · 2023Article
- Novel mutations in UMolecular therapy. Methods & clinical development · 2023Article
- Hybrid sequencing discloses unique aspects of the transcriptomic architecture in equid alphaherpesvirus 1.Heliyon · 2023Article
- Interactions of Equine Viruses with the Host Kinase Machinery and Implications for One Health and Human Disease.Viruses · 2023Review
- Anti-inflammatory compounds reduce equine herpesvirus type 1 replication and cell-to-cell spread.Frontiers in veterinary science · 2023Article
- Crystal structures of glycoprotein D of equine alphaherpesviruses reveal potential binding sites to the entry receptor MHC-I.Frontiers in microbiology · 2023Article
- Nanobody-based retargeting of an oncolytic herpesvirus for eliminating CXCR4Molecular therapy oncolytics · 2022Article
- Entry of Alphaherpesviruses.Current issues in molecular biology · 2021Review
- Lymphocystis Disease Virus (International journal of molecular sciences · 2020Article
- GBM-Targeted oHSV Armed with Matrix Metalloproteinase 9 Enhances Anti-tumor Activity and Animal Survival.Molecular therapy oncolytics · 2019Article
- Low-pH Endocytic Entry of the Porcine Alphaherpesvirus Pseudorabies Virus.Journal of virology · 2019Article
- EHV-1: A Constant Threat to the Horse Industry.Frontiers in microbiology · 2019Review
- Abortigenic but Not Neurotropic Equine Herpes Virus 1 Modulates the Interferon Antiviral Defense.Frontiers in cellular and infection microbiology · 2018Article
- Herpes simplex virus Membrane Fusion.Advances in anatomy, embryology, and cell biology · 2017Review
- Syncytial Mutations Do Not Impair the Specificity of Entry and Spread of a Glycoprotein D Receptor-Retargeted Herpes Simplex Virus.Journal of virology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Equine herpesvirus type 1 (EHV-1), a member of the Alphaherpesviridae, displays a broad host range in vitro, allowing for detailed study of the mechanisms of productive infection, including attachment and entry, in various cell culture systems. Previously, we showed that EHV-1 infects Chinese hamster ovary (CHO-K1) cells even though these cells do not express a known alphaherpesvirus entry receptor. In this report, we show by electron microscopy and an infectious recovery assay that entry into CHO-K1 cells occurs via an endocytic or phagocytic mechanism, while entry into equine dermal (ED) or rabbit kidney (RK13) cells occurs by direct fusion at the cell surface. In both cases (endocytic/phagocytic or direct fusion), entry leads to productive infection. Using drugs that inhibit clathrin-dependent or caveola-dependent endocytosis, we showed that EHV-1 entry into CHO-K1 cells does not require clathrin or caveolae. We also show that EHV-1 infection requires the activation of cell signaling molecules. In particular, we demonstrate that activation of the serine/threonine Rho kinase ROCK1 is critical for infection. Inhibition of this kinase by drugs or overexpression of a negative regulator of ROCK1 significantly blocked EHV-1 infection. These results show that EHV-1 can enter disparate cell types by at least two distinct mechanisms and that productive infection is dependent upon the activation of ROCK1.
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Registered trials
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.