Montreal, May 13, 2003 – Investigators at the Research Institute of the McGill University Health Centre (MUHC) have identified a gene that regulates the susceptibility to tuberculosis. This finding is published in this week's edition of the Proceedings of the National Academy of Sciences.
Tuberculosis, an infectious disease caused by the bacteria Mycobacterium tuberculosis, affects approximately 1.9 billion people worldwide. However, a large proportion of these individuals do not develop tuberculosis symptoms. Their body defense systems, or immune systems, are capable of controlling the growth of the bacteria.
"We have identified a gene that controls Mycobacterium tuberculosis growth in the lung," says MUHC microbiologist and senior author Dr. Philippe Gros. "This is an important step toward understanding why some infected individuals are able to fight off the infection and others are not. This discovery may lead to innovative prevention and treatment strategies for the 2 million patients who die from tuberculosis yearly."
Gros, also a professor of Biochemistry and Medicine at McGill University, along with his graduate student, Loukia Mitsosand, and his colleagues from the University of Oxford and the Trudeau Institute in Saranac Lake NY, used a mouse model and a technique called genome scanning to find the gene. They infected mice with air-borne bacteria and compared the DNA of those who were susceptible to infection with those who were not. A common gene variant on chromosome 19 was identified in those mice that were susceptible to infection. These mice had greater number of bacteria in their lungs and died earlier. "We believe that the gene variant, Trl-4, controls the growth of the bacteria in the lung. The next step is to test if this gene is present in humans who are susceptible to the disease," concludes Gros.
This study, funded by the National Institutes of Health, is available online at http://www.pnas.org.
The above story is based on materials provided by McGill University. Note: Materials may be edited for content and length.
Cite This Page: