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Physics professor puts flu-fighting drug to the test

By Dana Yates

Catherine Beauchemin

Up to 8,000 Canadians die every year from flu-related pneumonia. Ryerson researcher Catherine Beauchemin is studying why the influenza bug is more resistant to drugs and how treatment can be more effective.

Influenza – it’s the virus that public health officials dread, and according to a Ryerson University professor, the chief drug used to kill the flu isn’t as effective as ii used to be because the virus is always mutating.

For most people, influenza is largely a nuisance, interrupting personal and work lives for a few days. During that time, a fever, chills, cough, muscle aches and extreme fatigue are common. Some people, however, can become severely ill from this serious, acute respiratory illness, developing complications and possibly requiring hospitalization.

According to Health Canada, during a normal flu season, between 4,000 and 8,000 Canadians die from flu-related pneumonia. Most of the victims are seniors, who, along with children and those with chronic diseases such as HIV, are the most vulnerable to the influenza virus.  This annual cycle combined with fear of a flu pandemic such as the Spanish flu pandemic of 1918 are driving the world-wide scientific interest in flu research and concern over the timely development of anti-flu drugs to overcome the current resistance problem.

In the past, at-risk populations were typically prescribed the anti-viral drug amantadine when diagnosed with the flu.  Unfortunately, resistance to this drug has been on the rise. During the 2005-2006 flu season, 96 per cent of the influenza strains circulating in the general population were resistant to treatment with amantadine.  This situation prompted the American Centers for Disease Control and Prevention to recommend against future use of the medication.

In the hope of understanding how rapidly the flu virus can mutate to evade a drug, Catherine Beauchemin of Ryerson’s Department of Physics developed computer and mathematical models to simulate a flu infection. “If we can understand how rapidly the virus is mutating and why, we can start to answer questions such as how long it will take for the virus to become sensitive to the drug again if we stop using it for a while, or whether a different dosage could help prevent the emergence of drug resistance altogether,” says Dr. Beauchemin.

Dr. Beauchemin and her research colleagues created models to analyze how amantadine affects the course and outcome of a flu infection. The models simulate real experimental flu infections in which a cell culture is infected with the flu and the infection progresses, much like it would in a person. By comparing the experimental results against those of the models, the researchers were able to tease out unknown variables within the experimental data. In particular, the team determined that unlimited dosages of amantadine can block between 56 and 74 per cent of flu virus infection of cells. These findings differ from those typically reported in other experiments which range from 90 to 99 per cent blockage, depending on the flu strain.

“The reason for the difference is that the virus is always mutating,” says Dr. Beauchemin. “By the end of one round of treatment, a new drug-resistant strain would have developed. So, the low efficacy we found has nothing to do with the medication itself; it means the virus is mutating very rapidly to deke around the drug.”

To remedy the problem, medical researchers are now testing the effectiveness of drug cocktails, which have proven useful in treating HIV. “It’s doubtful that researchers will find an entirely new product that kills the flu virus any time soon,” says Dr. Beauchemin. “A cocktail of drugs is a more likely solution in the short term.”

Today, Dr. Beauchemin is using her models to study the emergence of drug resistance under different treatment strategies (different single drugs, drug cocktails, different dosage schedules). Her work may help advance efforts to develop an appropriate mix of flu-fighting drugs in the future.

The study was published in the May 2008 issue of the Journal of Theoretical Biology.  Funding for the project was provided in part by a Natural Sciences and Engineering Research Council of Canada Discovery Grant.

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