Scientists at UCLA’s Jonsson Comprehensive Cancer Center have demonstrated how viruses reprogram the metabolism of the cells they invade to promote continued viral growth within an organism. The findings could have implications for cancer treatments based on similarities between viruses and cancer-cell mechanisms and may even lead to drugs that could inhibit the virus that causes the common cold, the scientists say.
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| Adenovirus breaches a host cell’s outer defenses
to reach the nucleus and reprogram the cell’s
glucose metabolism. IIllustration: Jessica Byrne |
Previous research has shown that when normal cells become cancer cells, they are reprogrammed to act in certain ways that are very similar to virus-infected cells; the cells change their metabolism to support the maintenance and reproduction — and thus the spread — of the cancer. “In our laboratory, we’ve always been interested in how cancer cells acquire metabolic changes, compared to normal cells,” says Assistant Professor of Molecular and Medical Pharmacology Heather Christofk, PhD. “We decided to look at viruses and how they change the metabolism of cells they invade, because we thought they might be using mechanisms similar to those in cancer cells and that there might be some crossover in the way the mechanisms work.”
The researchers discovered that the adenovirus — the type of virus that causes the common cold — reprograms the cell it invades to be able to take on more glucose, an important nutrient for cells and viruses. The virus also instructs the cell to increase its use of the glucose to create energy and grow larger. These metabolic alterations enable the virus to begin replicating inside the cell.
“With this knowledge, we hope to begin designing drugs that can inhibit the increased glucose uptake in these cells,” says postdoctoral scholar Minh Thai, co-researcher on the project. “This could lead to drugs that stop the growth of viral infections, the most common being cold or flu, but also meningitis or some types of pneumonia. Then it might be possible to use the same kind of drug to stop the growth of cancer cells.”
“Adenovirus E4ORF1-Induced MYC Activation Promotes Host Cell Anabolic Glucose Metabolism and Virus Replication,” Cell Metabolism, April 1, 2014
