Canada Research Chair in Host Response to Virus Infection
Tier 1 - 2004-06-01
Identifying the genes underlying natural resistance and susceptibility to infection and characterizing gene products and their interactions to reconstruct pathways that go awry during certain viral infections.
The results have implications for identifying individuals at risk of developing disease following exposure to viruses, and for the design of anti-viral therapies.
Keeping Viruses at Bay: Lessons From Nature
Viral diseases rank among the most important burdens on human health, accounting for millions of deaths annually. Oddly, while some individuals are susceptible to infection, others seem naturally resistant. We know that the host's genetic makeup must play a role in such differences. If we could identify the "natural" resistance genes, we would have an entry point into molecular pathways that are activated to keep viruses at bay. This in turn would help us understand the interaction between host and pathogen and provide a basis for identifying specific therapeutic targets.
Identifying these resistance genes is the goal of geneticist Dr. Silvia Vidal. She studies how the host's genetic background affects the risk of infection and severity of disease following exposure to two particular human pathogens: cytomegalovirus (CMV) and coxsackievirus type 3 (CVB3). Infections due to these viruses are ubiquitous. In immunocompromised people, they cause potentially fatal disease; in others, they are implicated in arteriosclerosis, myocarditis, and dilated cardiomyopathy. Therapies primarily interfere with viral replication; neither vaccines nor definitive cures exist for either infection.
In 2001, Dr. Vidal identified an activating natural killer cell receptor gene as a major determinant of resistance to CMV. Owing to the gene's presence, natural killer cells can recognize and destroy CMV-infected cells. As a Canada Research Chair, Dr. Vidal continues to study the interaction between receptor and CMV, and between receptor and cellular components that participate in the killing of the infected cell. In addition, she is looking at the status of these receptors in immunocompromised patients presenting - or not - severe CMV-associated disease. She and her team have already localized additional genetic determinants of resistance to CMV and CVB3 infections that are being actively pursued for gene identification. No doubt, nature still has many more secrets to deliver.