Honors & News
February 25, 2013
Josh Munger, Ph.D. Discusses Jobs in Biochemistry and Biophysics with the Rochester Democrat and Chronicle
Joshua Munger was studying to become a veterinarian, but a microbiology requirement in college — in which he learned about the constant fight between host cells and the viruses that attack them — changed everything.
There's this evolutionary battle between the two,” he said. “I enjoyed learning about how they're always one-upping each other, how they're always trying to either cause infection or to limit the infection.
Munger, 37, has been an assistant professor in the Department of Biochemistry and Biophysics at the University of Rochester Medical Center since 2008. His work, which looks at how viral infection changes the metabolism of cells, has implications for cancer research and other areas.
January 14, 2010
Joshua Munger, Ph.D., an assistant professor of Biochemistry and Biophysics, has received a prestigious Damon Runyon Cancer Research Foundation Innovation Award, which recognizes promising early-career scientists who have outstanding research but lack sufficient preliminary data to get traditional funding.
Munger's research focuses on cancer cell metabolism. A virologist and biochemist by training, he is studying the metabolic activities that are altered when cells transform from normal to malignant. Whereas previous studies have focused narrowly on individual metabolic activities, Munger is taking a more global approach by examining the rates of numerous individual metabolic processes simultaneously.
September 29, 2008
Flu Virus with Envelope
Viruses dramatically increase cellular metabolism, and existing anti-obesity drugs may represent a new way to block these metabolic changes and inhibit viral infection, according to a study published today in the journal Nature Biotechnology.
Using new fluxomic techniques, our study reveals that viral infection takes control of cellular metabolism and drives, among other things, marked increases in fatty acid synthesis,said Joshua Munger, Ph.D., assistant professor of Biochemistry and Biophysics at the University of Rochester Medical Center, and a study author.
We also found that if you target these increases in fatty acid metabolism using existing anti-obesity and anti-metabolism drugs, you inhibit viral replication.
- The Human Cytomegalovirus UL26 Protein Antagonizes NF-κB Activation. J Virol. 88, 14289-300. (2014 Dec 15).
- Cytomegalovirus-mediated activation of pyrimidine biosynthesis drives UDP-sugar synthesis to support viral protein glycosylation. Proc Natl Acad Sci U S A. In press. (2014 Dec 03).
- Distinct domains within the human cytomegalovirus U(L)26 protein are important for wildtype viral replication and virion stability. PLoS One. 9, e88101. (2014 Jan 01).