ArticlePLoS pathogens2017
Integrated systems biology analysis of KSHV latent infection reveals viral induction and reliance on peroxisome mediated lipid metabolism.
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 47 papers.
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Who cites it
47 citing papers in PubMed, 68 citations in OpenAlex.
- The mitochondrial ubiquitin ligase MARCHF5 cooperates with MCL1 to inhibit apoptosis in KSHV-transformed primary effusion lymphoma cell lines.PLoS pathogens · 2026Article
- Metabolomic Analysis of Lytic KSHV Infection: Induced Host Nucleotide Metabolism Is Required for Infectious Virus Production.Viruses · 2026Article
- Global Lipidomic Analysis of Lytic KSHV Infection: The Lipid Chaperone FABP4 Supports Maximal Infectious Virion Production.Viruses · 2026Article
- Omics-Level Approaches to Studying Gammaherpesvirus Infection.Pathogens (Basel, Switzerland) · 2026Review
- PEX19 restricts porcine deltacoronavirus replication through farnesylation-dependent and -independent mechanisms.Journal of virology · 2026Article
- Global Lipidomic Analysis of Lytic KSHV Infection: The lipid chaperone FABP4 is required for maximal infectious virion production.bioRxiv : the preprint server for biology · 2026Article
- Remodeling of Metabolic and Secretory Organelles During Oncogenic and Oncomodulatory Viral Infections.Viruses · 2026Review
- A viral Cyclin D homolog protein hijacks the metabolic stress sensor SESN2 to promote primary effusion lymphoma growth.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Associative study of human herpesvirus 8 and Kaposi's sarcoma: Mapping viral oncogenic properties and the clinical scenario in oncological patients.Immunologic research · 2025Review
- Shaping Viral Infection Outcomes via Organelle Remodeling.Annual review of virology · 2025Review
- Understanding Metabolic Pathway Rewiring by Oncogenic Gamma Herpesvirus.Journal of microbiology and biotechnology · 2024Review
- Unveiling hidden connections in omics data via pyPARAGON: an integrative hybrid approach for disease network construction.Briefings in bioinformatics · 2024Article
- Current and future directions in network biology.Bioinformatics advances · 2024Article
- Association between arthropathies and postpartum hemorrhage: a bidirectional Mendelian randomization study.Frontiers in genetics · 2024Article
- A prospective cohort study identifies two types of HIV+ Kaposi Sarcoma lesions: proliferative and inflammatory.International journal of cancer · 2023Article
- Bcl-xL is required to protect endothelial cells latently infected with KSHV from virus induced intrinsic apoptosis.PLoS pathogens · 2023Article
- KSHV hijacks FoxO1 to promote cell proliferation and cellular transformation by antagonizing oxidative stress.Journal of medical virology · 2023Article
- Hepatitis C virus alters the morphology and function of peroxisomes.Frontiers in microbiology · 2023Article
- Peroxisomes and Viruses: Overview on Current Knowledge and Experimental Approaches.Methods in molecular biology (Clifton, N.J.) · 2023Review
- Fenofibrate for COVID-19 and related complications as an approach to improve treatment outcomes: the missed key for Holy Grail.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Kaposi's Sarcoma associated Herpesvirus (KSHV), an oncogenic, human gamma-herpesvirus, is the etiological agent of Kaposi's Sarcoma the most common tumor of AIDS patients world-wide. KSHV is predominantly latent in the main KS tumor cell, the spindle cell, a cell of endothelial origin. KSHV modulates numerous host cell-signaling pathways to activate endothelial cells including major metabolic pathways involved in lipid metabolism. To identify the underlying cellular mechanisms of KSHV alteration of host signaling and endothelial cell activation, we identified changes in the host proteome, phosphoproteome and transcriptome landscape following KSHV infection of endothelial cells. A Steiner forest algorithm was used to integrate the global data sets and, together with transcriptome based predicted transcription factor activity, cellular networks altered by latent KSHV were predicted. Several interesting pathways were identified, including peroxisome biogenesis. To validate the predictions, we showed that KSHV latent infection increases the number of peroxisomes per cell. Additionally, proteins involved in peroxisomal lipid metabolism of very long chain fatty acids, including ABCD3 and ACOX1, are required for the survival of latently infected cells. In summary, novel cellular pathways altered during herpesvirus latency that could not be predicted by a single systems biology platform, were identified by integrated proteomics and transcriptomics data analysis and when correlated with our metabolomics data revealed that peroxisome lipid metabolism is essential for KSHV latent infection of endothelial cells.
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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.