New approach to fight of virus

When a virus enters our body, an immune molecule called interferon are the first immune molecule to fight of the virus. Interferon is also know to suppress tumor growth and the effects of autoimmune diseases, this could help treat patients with multiple sclerosis and cancer. Sadly, some patients' bodies reject the foreign interferon or grow resistant to its effects.

Scientists from the University of Pennsylvania School of Veterinary Medicine's new research might offer a new way to fight of infections. The research states that, by targeting a certain molecule in the interferon signaling path, drugs that are especially designed may be able to boost the activity of a person's own interferon, augmenting the immune system's fight against viruses. There is a slight possibility that this same drugs may be effective at treating some types of cancer, multiple sclerosis, and certain autoimmune conditions.

Serge Fuchs, a professor of cell biology in Penn Vet's Department of Animal Biology and director of the School's Mari Lowe Comparative Oncology Center, was the senior author on the paper published in the Proceedings of the National Academy of Sciences.

"The practical significance of our study is a demonstration of the ability to use emerging pharmaceuticals to reactivate an individual's own interferon or to use a reduced dose to get the same effect," Fuchs said.

Christopher Carbone and Hui Zheng of the Department of Animal Biology and John Lewis and Alexander Reiter of the Department of Clinical Studies played leading roles in the study. Additional Penn Vet collaborators were Sabyasachi Bhattacharya, Paula Henthorn and Kendra Bence. Zhong-Yin Zhang of Indiana University School of Medicine and Darren Baker of Biogen Idec also contributed.

The research was only made possible since the team decided to approach this study by doing a comparative-medicine approach. In their approach 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 been chosen to be the model organism of choice for such a study, but they lack a molecular element of the interferon pathway that humans and cat 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 tackles virus by attaching to an interferon receptor on cells, this triggers a cascade of other molecular events and leading to the production of proteins  that prevent the virus from reproducing or that stimulate other immune responses. 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.

The researchers were not on a search to discover a new drug, as a matter of fact they were attempting to solve a paradox of cell biology.

Next, they plan on using their new discovery in a model of feline immunodeficiency virus, or the cat version of AIDS, to see if its virus-fighting capabilities have an effect against an infection.

The study was supported by the National Institutes of Health and the Mari Lowe Center for Comparative Oncology Research at the University of Pennsylvania.

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Reference: Science Daily (11/09/12)