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Metabolism goes viral
Shigeki J Miyake-Stoner1, Clodagh C O'Shea1
1Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037-1099, USA.
Abstract:
Viral and cellular oncogenes converge in targeting critical protein interaction networks to reprogram the cellular DNA and protein replication machinery for pathological replication. In this issue, Thai et al. (2014) show that adenovirus E4ORF1 activates MYC glycolytic targets to induce a Warburg-like effect that converts glucose into nucleotides for viral replication.
Insights
Adenovirus E4ORF1 activates MYC to promote a Warburg-like effect, reprogramming glucose metabolism for viral replication. This study reveals how viral proteins hijack cellular pathways to fuel pathological processes.
Area of Science:
- Molecular Biology
- Virology
- Cancer Biology
Background:
- Viral and cellular oncogenes reprogram host cell machinery for replication.
- Oncogenes target protein interaction networks to alter cellular functions.
Purpose of the Study:
- To investigate the mechanism by which adenovirus E4ORF1 interacts with MYC.
- To understand how E4ORF1-induced MYC activation affects cellular metabolism.
Main Methods:
- Analysis of adenovirus E4ORF1 protein.
- Study of MYC glycolytic targets.
- Investigation of cellular glucose metabolism.
Main Results:
- Adenovirus E4ORF1 activates MYC's glycolytic targets.
- This activation induces a Warburg-like metabolic effect.
- Glucose is converted into nucleotides to support viral replication.
Conclusions:
- Adenovirus E4ORF1 hijacks MYC to reprogram cellular metabolism.
- The Warburg-like effect provides essential nucleotides for viral replication.
- This highlights a convergence of viral and cellular oncogenic pathways.
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