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A comparative medicine study by Penn vet identifies a new approach to combat viral infections
Date:11/9/2012

he team's comparative-medicine approach, in which they examined the effects of activating the interferon pathway in both human cells and in cats affected by a naturally occurring disease. Mice would normally be the model organism of choice for such a study, but they lack a molecular element of the interferon pathway that humans and cats share.

"Mice are very convenient, but they may not always recapitulate human diseases that well," Fuchs said. "Veterinary diseases happen naturally, and they provide a less convenient but a more truthful recapitulation of the human situation."

Interferon fights viruses by binding to an interferon receptor on cells, triggering a cascade of other molecular events and leading to the production of proteins that prevent viruses from reproducing or that stimulate other immune responses. But because too much interferon can harm the host's body, this signaling cascade has a built-in brake: Using a separate molecular pathway, interferon triggers the body's cells to remove its own receptor, so the immune system attack doesn't go on indefinitely.

"It's very important to understand what regulates the responsiveness of cells to interferon, and a major factor is the levels of cell-surface receptors," Fuchs said.

Although the researchers' investigations of these pathways led them to identify a target for improving the body's virus-fighting ability, they didn't set out to discover a drug. Rather, they were attempting to solve a paradox of cell biology.

The paradox rests on the fact that many steps in the interferon-signaling pathway involve adding a molecule of phosphate to proteins in the cascade. Interferon itself promotes the addition of phosphate onto the interferon receptor, yet previous evidence suggested that the receptor resisted being removed by the cell if it had phosphate added. Given that interferon does in fact trigger the removal of its own receptor, the research team hypothesized that an
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Contact: Katherine Unger Baillie
kbaillie@upenn.edu
215-898-9194
University of Pennsylvania
Source:Eurekalert

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