Great study. Normally when our bodies fight off viral infections, they use interferon as means to stop the virus from replicating. Moreover, interferon starts an immune response against the virus. The very interesting part is, that our bodies don't continue this response forever. After a certain amount of time, interferon triggers its own disarming by removing the interferon receptor of the cells. As soon as this happens, the interferon induced attack stops. Who is responsible? A single enzyme called tyrosine phosphatase 1 B leads to the removal of interferon receptors. PTP1B inhibitors were a main focus in the fight on obesity and diabetes. It would be interesting to know if there are still some in the pipeline and if we can see some approval soon. When administered to human cells, that were infected with Hepatitis C or stomatitis virus, even small amounts of interferon successfully stopped the virus from reproducing. It would be so interesting to know, if PWCs have normal presence of interferon receptors on their cells. Maybe a chronic viral infection leads to interferon production, the interferon slowly triggers a disappearance of interferon receptors. The virus then keeps replicating, does harm but cannot be cleared because all new interferon has no receptor to bind on. http://www.sciencedaily.com/releases/2012/11/121109162020.htm ScienceDaily (Nov. 9, 2012) — When a virus such as influenza invades our bodies, interferon proteins are among the first immune molecules produced to fight off the attack. Interferon can also play a role in suppressing tumor growth and the effects of autoimmune diseases, and doctors may use an artificial form of interferon to treat patients with certain cancers or multiple sclerosis. But even this approach sometimes fails when patients' bodies reject the foreign interferon or growing resistant to its effects. A study by scientists from the University of Pennsylvania School of Veterinary Medicine offers a new strategy for enhancing the effects of interferon in fighting off infection. The research suggests that, by targeting a particular molecule in the interferon signaling pathway, specially designed drugs may be able to boost the activity of a person's own interferon, augmenting the immune system's fight against viruses. It's possible that the same drugs might also be effective against some types of cancer 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. ... 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. ... Using human cells infected with hepatitis C, the researchers found that adding a PTP1B inhibitor allowed smaller doses of interferon to be effective in keeping the virus from reproducing. They demonstrated a similar effect in human cells infected with vesicular stomatitis virus. ... , they examined five cats that had been enrolled by their owners in the study. Each was suffering from chronic stomatitis, a condition that involves substantial inflammation in the mouth and makes it painful for the cats to eat and groom. The cats received a single injection of a PTP1B inhibitor. Two weeks later, all five showed noticeable reductions in redness and inflammation, providing clinical evidence that these drugs could be used to treat infection. Fuchs said that what seemed like a drawback in the study -- that it couldn't be effectively modeled in mice -- ended up being a benefit, as naturally occurring diseases in animals such as cat and dogs more closely mimic many human diseases. Because interferon is known to suppress tumors and help multiple sclerosis patients, the results of this study give the researchers optimism that PTP1B could be a target for anti-cancer and anti-autoimmune disease therapies. As a next step, they plan to test the PTP1B inhibitors in a model of feline immunodeficiency virus, or the cat version of AIDS, to see if its virus-fighting capabilities can have an effect against that 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.