ArticleCell host & microbe2013
A unique herpesviral transcriptional program in KSHV-infected lymphatic endothelial cells leads to mTORC1 activation and rapamycin sensitivity.
Article in Cell host & microbe, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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Who cites it
87 citing papers in PubMed, 117 citations in OpenAlex.
- Systemically circulating viral and tumor-derived microRNAs in KSHV-associated malignancies.PLoS pathogens · 2013Trial
- Endostemonine I as a Multi-Target Inhibitor of Kaposi's Sarcoma-Associated Herpesvirus Oncogenic Pathways: An Integrative Computational Study.Medical sciences (Basel, Switzerland) · 2026Article
- ORF45-induced Filamin A phosphorylation promotes cell motility and cell-contact dependent viral infection of Kaposi's sarcoma-associated herpesvirus.PLoS pathogens · 2025Article
- Model Systems of Gammaherpesvirus Infection, Immunity, and Disease.Journal of medical virology · 2025Review
- Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus.Journal of visualized experiments : JoVE · 2025Article
- Heterogeneous Activation of Signaling Pathways and Therapeutic Vulnerabilities in KSHV-Associated Primary Effusion Lymphoma Cell Lines.Journal of medical virology · 2025Article
- Kaposi's sarcoma-associated herpesvirus induces mitochondrial fission to evade host immune responses and promote viral production.Nature microbiology · 2025Article
- The immune sensitivity caused by DUSP11, an RNA 5'-end maturation phosphatase, is adjusted by a human non-coding RNA, nc886.Cellular and molecular life sciences : CMLS · 2025Article
- The pathogen's playbook in cancer: from oncogenesis to progression.Frontiers in oncology · 2025Review
- FoxK1 and FoxK2 cooperate with ORF45 to promote late lytic replication of Kaposi's sarcoma-associated herpesvirus.Journal of virology · 2024Article
- BiP/GRP78 is a pro-viral factor for diverse dsDNA viruses that promotes the survival and proliferation of cells upon KSHV infection.PLoS pathogens · 2024Article
- Beyond the Gut: The intratumoral microbiome's influence on tumorigenesis and treatment response.Cancer communications (London, England) · 2024Review
- Mapping herpesvirus-driven impacts on the cellular milieu and transcriptional profile of Kaposi sarcoma in patient-derived mouse models.bioRxiv : the preprint server for biology · 2024Article
- Article
- miR-769-3p inhibits cellular proliferation of KSHV-infected SH-SY5Y cells through targeting mTOR.Journal of Cancer · 2024Article
- Hypoxia and hypoxia-inducible factors in Kaposi sarcoma-associated herpesvirus infection and disease pathogenesis.Journal of medical virology · 2023Review
- Polypharmacology-based kinome screen identifies new regulators of KSHV reactivation.PLoS pathogens · 2023Article
- Inhibition of AIM2 inflammasome activation by SOX/ORF37 promotes lytic replication of Kaposi's sarcoma-associated herpesvirus.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Onco-Pathogen Mediated Cancer Progression and Associated Signaling Pathways in Cancer Development.Pathogens (Basel, Switzerland) · 2023Review
- The Kaposi's sarcoma progenitor enigma: KSHV-induced MEndT-EndMT axis.Trends in molecular medicine · 2023Review
27 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Immunosuppression therapy following organ transplantation is a significant factor in the development and progression of Kaposi's sarcoma-associated herpesvirus (KSHV)-induced posttransplant Kaposi's sarcoma (KS). Switching from cyclosporine to the mTOR inhibitor rapamycin is reported to promote KS regression without allograft rejection. Examining the underlying molecular basis for this clinical observation, we find that KSHV infection selectively upregulates mTOR signaling in primary human lymphatic endothelial cells (LECs), but not blood endothelial cells (BECs), and sensitizes LECs to rapamycin-induced apoptosis. Viral transcriptome analysis revealed that while infected BECs display conventional latency, KSHV-infected LECs support a radically different program involving widespread deregulation of both latent and lytic genes. ORF45, a lytic gene selectively expressed in infected LECs, is required for mTOR activation and critical for rapamycin sensitivity. These studies reveal the existence of a unique herpesviral gene expression program corresponding to neither canonical latency nor lytic replication, with important pathogenetic and therapeutic consequences.
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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.