Related Experiment Video
Updated: May 28, 2026
11:28
Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
Targeting Host Metabolic and Epigenetic Rewiring Blocks Lytic Gammaherpesvirus Production
Morgan C Jones1,2, Tina M Le3, Connor J Mahoney1,2
1Department of Biochemistry, University of Washington School of Medicine, Seattle, WA 98195, USA.
Viruses
|May 27, 2026
Summary
Murine gammaherpesvirus 68 infection alters host cell metabolism and gene expression. Targeting the pentose phosphate pathway (PPP) and Ten-Eleven Translocation (TET) enzymes inhibits viral production.
Area of Science:
- Virology
- Molecular Biology
- Metabolic Engineering
Background:
- Gammaherpesviruses are oncogenic and reprogram host cell metabolism for viral replication.
- Murine herpesvirus 68 (MHV-68) is a model for studying lytic gammaherpesvirus infections and host cell alterations.
Purpose of the Study:
- To characterize host transcriptional changes during MHV-68 infection.
- To identify novel host pathways for therapeutic targeting in gammaherpesvirus infections.
Main Methods:
- Temporal bulk RNA-sequencing of mock- and MHV-68-infected NIH 3T3 cells.
- Pharmacological inhibition of the pentose phosphate pathway (PPP) and Ten-Eleven Translocation (TET) enzymes.
Main Results:
- MHV-68 infection induced widespread host gene expression changes, including innate immunity and metabolic pathways.
- Activation of the PPP and increased PPP metabolites were observed.
- Inhibition of PPP (using 6-AN) and TET activity reduced infectious MHV-68 production.
Conclusions:
- A novel metabolic-epigenetic crosstalk supports gammaherpesvirus replication.
- Host pathways, including the PPP and TET enzymes, are potential therapeutic targets for gammaherpesvirus infections.
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