ArticlePLoS pathogens2017
The Kaposi's sarcoma-associated herpesvirus (KSHV) non-structural membrane protein K15 is required for viral lytic replication and may represent a therapeutic target.
Article in PLoS pathogens, 2017. 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, 35 citations in OpenAlex.
- Host microRNA-31-5p regulates KHDRBS3 expression and modulates viral gene expression during KSHV lytic reactivation.Cell reports · 2026Article
- Genome evolution of Kaposi sarcoma-associated herpesvirus (KSHV).Journal of virology · 2025Article
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- Endothelial Cells Stably Infected with Recombinant Kaposi's Sarcoma-Associated Herpesvirus Display Distinct Viscoelastic and Morphological Properties.Cellular and molecular bioengineering · 2025Article
- Review
- Modulation of Lymphotoxin β Surface Expression by Kaposi's Sarcoma-Associated Herpesvirus K3 Through Glycosylation Interference.Journal of medical virology · 2025Article
- Unearthing the role of septins in viral infections.Bioscience reports · 2024Review
- Antibody profiling and predictive modeling discriminate between Kaposi sarcoma and asymptomatic KSHV infection.PLoS pathogens · 2024Article
- Membrane-bound Merkel cell polyomavirus middle T protein constitutively activates PLCγ1 signaling through Src-family kinases.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Today's Kaposi sarcoma is not the same as it was 40 years ago, or is it?Journal of medical virology · 2023Review
- Cancers associated with human gammaherpesviruses.The FEBS journal · 2022Review
- Genome-wide regulation of KSHV RNA splicing by viral RNA-binding protein ORF57.PLoS pathogens · 2022Article
- Human Gammaherpesvirus 8 Oncogenes Associated with Kaposi's Sarcoma.International journal of molecular sciences · 2022Review
- Kaposi Sarcoma, a Trifecta of Pathogenic Mechanisms.Diagnostics (Basel, Switzerland) · 2022Review
- Kaposi's Sarcoma-Associated Herpesvirus, the Etiological Agent of All Epidemiological Forms of Kaposi's Sarcoma.Cancers · 2021Review
- Recruitment of phospholipase Cγ1 to the non-structural membrane protein pK15 of Kaposi Sarcoma-associated herpesvirus promotes its Src-dependent phosphorylation.PLoS pathogens · 2021Article
- Review
- Epigenetic control in Kaposi sarcoma-associated herpesvirus infection and associated disease.Seminars in immunopathology · 2020Review
- Targeting Kaposi's Sarcoma-Associated Herpesvirus ORF21 Tyrosine Kinase and Viral Lytic Reactivation by Tyrosine Kinase Inhibitors Approved for Clinical Use.Journal of virology · 2020Article
- Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) is the infectious cause of the highly vascularized tumor Kaposi's sarcoma (KS), which is characterized by proliferating spindle cells of endothelial origin, extensive neo-angiogenesis and inflammatory infiltrates. The KSHV K15 protein contributes to the angiogenic and invasive properties of KSHV-infected endothelial cells. Here, we asked whether K15 could also play a role in KSHV lytic replication. Deletion of the K15 gene from the viral genome or its depletion by siRNA lead to reduced virus reactivation, as evidenced by the decreased expression levels of KSHV lytic proteins RTA, K-bZIP, ORF 45 and K8.1 as well as reduced release of infectious virus. Similar results were found for a K1 deletion virus. Deleting either K15 or K1 from the viral genome also compromised the ability of KSHV to activate PLCγ1, Erk1/2 and Akt1. In infected primary lymphatic endothelial (LEC-rKSHV) cells, which have previously been shown to spontaneously display a viral lytic transcription pattern, transfection of siRNA against K15, but not K1, abolished viral lytic replication as well as KSHV-induced spindle cell formation. Using a newly generated monoclonal antibody to K15, we found an abundant K15 protein expression in KS tumor biopsies obtained from HIV positive patients, emphasizing the physiological relevance of our findings. Finally, we used a dominant negative inhibitor of the K15-PLCγ1 interaction to establish proof of principle that pharmacological intervention with K15-dependent pathways may represent a novel approach to block KSHV reactivation and thereby its pathogenesis.
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