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Vaccinia Reporter Viruses for Quantifying Viral Function at All Stages of Gene Expression
Published on: May 15, 2014
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Vaccinia virus requires glutamine but not glucose for efficient replication
Krystal A Fontaine1, Roman Camarda, Michael Lagunoff
1Department of Microbiology, University of Washington, Seattle, Washington, USA.
Journal of Virology
|February 7, 2014
Summary
Vaccinia virus (VACV) redirects host cell metabolism, relying on glutamine for replication instead of glucose. Inhibiting glutamine metabolism significantly reduces viral protein synthesis and production, offering a potential antiviral target.
Area of Science:
- Virology
- Cellular Metabolism
- Biochemistry
Background:
- Viruses depend on host cell metabolism for energy and building blocks.
- Vaccinia virus (VACV), a poxvirus, historically significant for smallpox eradication.
- Previous studies lacked detailed metabolic analysis of poxvirus infections.
Purpose of the Study:
- To investigate how VACV infection alters host cell metabolism.
- To identify the specific metabolic pathways crucial for VACV replication.
- To provide the first metabolomic analysis of a poxvirus infection.
Main Methods:
- Global metabolic screening of VACV-infected human fibroblasts.
- Deprivation of exogenous glutamine and glucose in infected cells.
- Inhibition of glutaminolysis and rescue with tricarboxylic acid (TCA) cycle intermediates.
Main Results:
- VACV infection significantly alters host cell metabolism, prioritizing glutamine over glucose.
- Glutamine deprivation drastically reduces infectious virus production and protein synthesis.
- Inhibition of glutaminolysis impairs viral replication, but can be rescued by TCA cycle intermediates.
Conclusions:
- VACV uniquely utilizes glutamine to maintain the TCA cycle for anaplerosis.
- VACV infection establishes a distinct carbon utilization program.
- Targeting glutamine metabolism presents a potential strategy for antiviral therapies against poxviruses.
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