Cell-mediated immune responses in cytomegalovirus-induced myocarditis [ 2000 - 2002 ]

Also known as: The host's immunity to virus triggered heart disease

Research Grant

[Cite as]

Researchers: Cassandra James (Formerly Lawson) (Principal investigator)

Brief description The proposed research will provide a clearer understanding of the body's immune response to virus and self tissues in inflammatory heart disease. Inflammation of the heart, myocarditis, can occur following virus infection. The condition may be chronic and persist for a long time even after the virus infection has resolved. The autoimmune response attacks the body's own tissues and involves reactivity to a heart protein, namely myosin. Important immune cells (B and T cells) play a role in the disease process. Antibodies are produced by B cells during the virus infection which react to myosin but we do not know the reactivity of T cells in this disease. Natural molecules (cytokines) produced by our body are important for shaping our immune response (T and B cell-mediated) in virus infections and diseases. Autoimmune disease is a result of a mistake by our immune system. Such diseases can be triggered by virus infection and require immunotherapy for correction. In the project, we propose to : 1. Investigate immunological responses of immune cells (T cells) in the heart using an experimental mouse model of cardiovascular disease. 2. Examine the response of T cells to myosin using the mouse model of infection with a herpesvirus, cytomegalovirus (CMV). 3. Study the role of cytokines and immunotherapy in our CMV-triggered myocarditis model. Determination of the events leading to cardiovascular disease will allow developments of improved treatment and potential vaccinations against inflammatory heart disease. The findings from the proposed project are expected to have broader impact for other viruses invading the heart and their associated diseases in man.

Funding Amount $AUD 238,407.91

Funding Scheme NHMRC Project Grants

Notes Standard Project Grant

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