Related Experiment Video
Updated: May 11, 2025
07:02
Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
Published on: September 14, 2010
12.5K
Analysis of Metabolomic Reprogramming Induced by Infection with Kaposi's Sarcoma-Associated Herpesvirus Using
Abdulkarim Alfaez1,2, Michael W Christopher3, Timothy J Garrett1,3
1Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, College of Medicine, Gainesville, FL 32610, USA.
International Journal of Molecular Sciences
|April 17, 2025
Summary
Kaposi's sarcoma-associated herpesvirus (KSHV) rapidly alters oral epithelial cell metabolism. This study identified key metabolic changes, offering potential targets for new antiviral therapies against KSHV infection.
Area of Science:
- Virology
- Metabolomics
- Cellular Biology
Background:
- Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic virus lacking vaccines or antiviral treatments.
- Understanding KSHV's manipulation of host cell metabolism is crucial for developing targeted therapies.
- Lytic infection is a key stage for viral spread that may be influenced by metabolic alterations.
Purpose of the Study:
- To investigate the rapid metabolic changes in oral epithelial cells upon KSHV infection.
- To identify specific metabolic pathways and metabolites affected by KSHV.
- To provide insights into potential therapeutic targets for KSHV infection.
Main Methods:
- Untargeted metabolomic analysis was performed on KSHV-infected and mock-infected telomerase-immortalized gingival keratinocytes (TIGK) at 4 hours post-infection.
- Differential metabolic features were quantified and analyzed between the two groups.
- Associated metabolic pathways were identified.
Main Results:
- KSHV infection significantly altered the metabolomic landscape of TIGK cells.
- A total of 804 differential metabolic features were detected, with 741 metabolites upregulated and 63 downregulated.
- Key affected metabolites included ornithine, arginine, putrescine, glutamate, and glutamine, linked to pathways like the urea cycle and de novo pyrimidine synthesis.
Conclusions:
- KSHV infection induces rapid and significant metabolic reprogramming in oral epithelial cells.
- These metabolic alterations may play a role in promoting KSHV lytic replication and transmission.
- The identified metabolic pathways represent potential targets for future KSHV antiviral therapies.
