Host-pathogen molecular and cardiovascular interaction during influenza infection

本研究旨在更好地了解心血管生理学、生物标志物和病毒基因组 在正常和不同炎症性疾病期间从流感感染发作到恢复的异质性变化 国家（肥胖和抗病毒治疗）。彻底调查时空炎症 生物标志物谱沿着呼吸和心血管生理谱，从幼稚到 恢复将使我们能够探索在原发部位对流感感染的反应之间的相互作用， 感染及其周边影响。新生物标志物的鉴定（分子和蛋白质组学） 可以显著改善对心血管事件的预测。 此外，对复制型流感人群进行更彻底的基因组研究可以更好地 监测和预测正在发生和正在出现的事件。这项研究将调查一个主要的差距， 通过详细分析心血管和分子变化， 局部呼吸道病毒感染伴肥胖和抗病毒治疗或化学预防。我们希望 用以下药物缓解呼吸道病毒感染引起的心血管事件（期间和之后） 肥胖小鼠的促炎状态或炎症事件的及时减少， 奥司他韦治疗时机。我们的期望是确定在流感期间存在的标志物， 病毒感染与疾病和生理稳态的变化相关， 炎症状态（肥胖引起的促炎和抗病毒药引起的抗炎）。 总的来说，我们假设，在呼吸系统局部炎症事件引起的， 流感病毒感染导致正常心血管生理学、生物标志物和 病毒基因组的异质性可以通过肥胖和及时接受抗病毒治疗来改变。

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.