ArticleJournal of virology2018
A Kaposi's Sarcoma-Associated Herpesvirus Infection Mechanism Is Independent of Integrins α3β1, αVβ3, and αVβ5.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Monoclonal neutralizing antibodies elicited by infection with Kaposi sarcoma-associated herpesvirus reveal critical sites of vulnerability on gH/gL.PLoS pathogens · 2026Article
- Eph receptor tyrosine kinases are functional entry receptors for murine gammaherpesvirus 68.PLoS pathogens · 2025Article
- Quantitative proteomic analysis of PK-15 cells infected with porcine circovirus type 3 using 4D-DIA approach.Veterinary research communications · 2024Article
- Kaposi sarcoma-associated herpesvirus complement control protein (KCP) and glycoprotein K8.1 are not required for viral infectionJournal of virology · 2024Article
- Epigenetic and epitranscriptomic regulation during oncogenicFrontiers in microbiology · 2024Review
- EPHA2 Receptor as a Possible Therapeutic Target in Viral Infections.Current medicinal chemistry · 2024Review
- Plxdc family members are novel receptors for the rhesus monkey rhadinovirus (RRV).PLoS pathogens · 2021Article
- The structural basis of herpesvirus entry.Nature reviews. Microbiology · 2021Review
- Cellular Receptors Involved in KSHV Infection.Viruses · 2021Review
- The Role of the Eph Receptor Family in Tumorigenesis.Cancers · 2021Review
- Molecular basis of EphA2 recognition by gHgL from gammaherpesviruses.Nature communications · 2020Article
- Epstein-Barr Virus gH/gL and Kaposi's Sarcoma-Associated Herpesvirus gH/gL Bind to Different Sites on EphA2 To Trigger Fusion.Journal of virology · 2020Article
- A Recombinant Rhesus Monkey Rhadinovirus Deleted of Glycoprotein L Establishes Persistent Infection of Rhesus Macaques and Elicits Conventional T Cell Responses.Journal of virology · 2020Article
- Towards Understanding KSHV Fusion and Entry.Viruses · 2019Review
- Epithelial cell infection by Epstein-Barr virus.FEMS microbiology reviews · 2019Article
- CRISPR/Cas9-Mediated Knockout andJournal of virology · 2019Article
- Kaposi Sarcoma-Associated Herpesvirus Glycoprotein H Is Indispensable for Infection of Epithelial, Endothelial, and Fibroblast Cell Types.Journal of virology · 2019Article
- EphA7 Functions as Receptor on BJAB Cells for Cell-to-Cell Transmission of the Kaposi's Sarcoma-Associated Herpesvirus and for Cell-Free Infection by the Related Rhesus Monkey Rhadinovirus.Journal of virology · 2019Article
- EphA2 Is a Neutrophil Receptor for Candida albicans that Stimulates Antifungal Activity during Oropharyngeal Infection.Cell reports · 2019Article
- Ephrin Receptor A4 is a New Kaposi's Sarcoma-Associated Herpesvirus Virus Entry Receptor.mBio · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host receptor usage by Kaposi's sarcoma-associated herpesvirus (KSHV) has been best studied using primary microvascular endothelial and fibroblast cells, although the virus infects a wide variety of cell types in culture and in natural infections. In these two infection models, KSHV adheres to the cell though heparan sulfate (HS) binding and then interacts with a complex of EphA2, xCT, and integrins α3β1, αVβ3, and αVβ5 to catalyze viral entry. We dissected this receptor complex at the genetic level with CRISPR-Cas9 to precisely determine receptor usage in two epithelial cell lines. Surprisingly, we discovered an infection mechanism that requires HS and EphA2 but is independent of αV- and β1-family integrin expression. Furthermore, infection appears to be independent of the EphA2 intracellular domain. We also demonstrated that while two other endogenous Eph receptors were dispensable for KSHV infection, transduced EphA4 and EphA5 significantly enhanced infection of cells lacking EphA2.
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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.