Metabolic Hijacking
Viruses are obligate parasites that depend entirely on host cell resources for replication. To meet their biosynthetic demands, viruses reprogram host cell metabolism—a process we call "metabolic hijacking."
Understanding these metabolic changes reveals vulnerabilities that can be exploited for antiviral therapy. By targeting virus-induced metabolic pathways rather than viral proteins directly, we can potentially develop broad-spectrum antivirals effective against multiple viruses.
Research Focus Areas
Energy Metabolism
Viruses dramatically alter cellular energy production, often shifting cells toward glycolysis even in the presence of oxygen (the Warburg effect). We study:
- Viral manipulation of glycolysis and the TCA cycle
- Mitochondrial function during infection
- ATP dynamics and viral replication
Lipid Metabolism
Lipids are essential for viral membrane formation, replication complexes, and virion assembly:
- Fatty acid synthesis during infection
- Phospholipid remodeling
- Cholesterol metabolism and viral entry
Nucleotide Metabolism
Viral genome replication requires massive nucleotide pools:
- De novo nucleotide synthesis
- Salvage pathway utilization
- Targeting nucleotide metabolism for antivirals
Experimental Approaches
- Mass spectrometry-based metabolomics
- Stable isotope tracing
- Real-time metabolic flux analysis
- CRISPR screens for metabolic dependencies
- Advanced imaging of metabolic processes