Anti-viral CD8+ T-cell responses are critical for the eradication of acute viral infections and the control of chronic viral infections. However, in chronic viral infections, their functions is impaired. Moreover, we have found generalized or bulk CD8+ T-cell dysfunction in chronic Hepatitis C infection, which may bear consequences for overall health status beyond that directly caused by HCV.
Strong partnerships with clinician-scientists help us access clinical samples from HCV mono- and HIV-CV co-infected individuals. Specifically, Dr. Curtis Cooper (Director of the Ottawa Hospital and Regional Hepatitis Program, Ottawa Hospital) is a primary collaborator for our research program.
In addition, international collaborations are ongoing for the study of cytokine receptor expression in an animal model of HIV infection (i.e. simian immunodeficiency virus infection of rhesus macaques) as well as immunogenotyping in HCV infection.
Identify the underlying mechanisms of CD8+ T-cell dysfunction in HCV mono- and HIV-HCV co-infection. The function of CD8+ T-cells in the blood and liver are being evaluated. Both host and viral factors that contribute to bulk CD8+ T-cell impairment are being studied.
Evaluate innate and adaptive immunity interactions in HCV infection, specifically between macrophage subsets, liver-resident macrophages (Kupffer cells) and CD8+ T-cells.
Evaluate the effects of chronic HCV infection on responses to routine vaccination (e.g. seasonal flu and Hepatitis B vaccines).
Explore the therapeutic potential of soluble cytokine receptors in the prevention and treatment of disease.