Host-pathogen molecular and cardiovascular interaction during influenza infection

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This study is aimed to better understand cardiovascular physiological, biomarker, and viral genomic heterogeneity changes from influenza infection onset to recovery during normal and differing inflammatory states (obesity and antiviral treatment). Thorough investigation of the spatiotemporal inflammatory biomarker profile along with the respiratory and cardiovascular physiological profiles from naivety to recovery will allow us to explore the interplay between responses to influenza infection in primary site of infection and its peripheral effects. The identification of novel biomarkers (molecular and proteomic) during an inflammatory event could significantly improve predictions for cardiovascular events. Additionally, more thorough genomic investigation of replicating influenza populations can lead to better surveillance and prediction of ongoing and emerging events. This study will investigate a major gap in knowledge by performing detailed analysis of cardiovascular and molecular changes associated with localized respiratory viral infection with obesity and antiviral treatment or chemoprophylaxis. We hope to modify cardiovascular events caused by respiratory virus infection (both during and after) with pro-inflammatory state of obese mice or reduction of inflammatory events in a timely manner with varying oseltamivir treatment timings. The expectation is to define markers that are present during an influenza virus infection that correlate with disease and changes in physiological homeostasis specifically for each inflammatory state (proinflammatory caused by obesity and anti-inflammatory caused by antivirals). Overall, we hypothesize that a localized inflammatory event in the respiratory system caused by the influenza virus infection leads systemic changes in normal cardiovascular physiology, biomarkers, and viral genomic heterogeneity that can be altered by obesity and timely admission of antiviral therapeutics.