Grant: CIHR Fellowship

Cardiovascular diseases including myocardial infarction, or heart attack, continue to claim an increasing number of lives worldwide, while influenza A virus infection, the major causative agent of the flu, is responsible for recurring pulmonary infections and substantial global mortality. Importantly, influenza infection also augments susceptibility to heart attack. Yet, the reasons for this and how it occurs are unknown. Understanding why is of great value, as both influenza and cardiovascular disease are significant threats to human health with limited therapeutic strategies. Even though flu infections are constrained to the lungs, anti-influenza type I IFN signalling can transcriptionally imprint monocytes in the bone marrow to enhance immune responses in peripherally inflamed tissues. Although type I IFN is protective against influenza, it also increases susceptibility to heart attack by promoting detrimental inflammation in the heart. Therefore, it is the goal of this project to investigate a potential link between influenza-induced type I IFN signalling in the bone marrow and detrimental inflammatory monocyte responses during myocardial infarction, which underlies the enhanced severity. The findings of this study will provide better knowledge of the risk factors of cardiovascular disease and could lead to improved clinical interventions.