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Influenza virus lung infection protects from respiratory syncytial virus-induced immunopathology

机译:流感病毒肺部感染可防止呼吸道合胞病毒诱导的免疫病理学

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摘要

The effect of infection history is ignored in most animal models of infectious disease. The attachment protein of respiratory syncytial virus (RSV) induces T helper cell type 2-driven pulmonary eosinophilia in mice similar to that seen in the failed infant vaccinations in the 1960s. We show that previous influenza virus infection of mice: (a) protects against weight loss, illness, and lung eosinophilia; (b) attenuates recruitment of inflammatory cells; and (c) reduces cytokine secretion caused by RSV attachment protein without affecting RSV clearance. This protective effect can be transferred via influenza-immune splenocytes to naive mice and is long lived. Previous immunity to lung infection clearly plays an important and underestimated role in subsequent vaccination and infection. The data have important implications for the timing of vaccinations in certain patient groups, and may contribute to variability in disease susceptibility observed in humans.
机译:在大多数传染病动物模型中,都忽略了感染史的影响。呼吸道合胞病毒(RSV)的附着蛋白在小鼠中诱导T型辅助细胞2型驱动的肺嗜酸性粒细胞增多,类似于1960年代婴儿接种失败的情况。我们证明了以前的小鼠流感病毒感染:(a)防止体重减轻,疾病和肺嗜酸性粒细胞增多; (b)减轻炎症细胞的募集; (c)减少由RSV附着蛋白引起的细胞因子分泌,而不影响RSV清除率。这种保护作用可以通过对流行性感冒免疫的脾细胞转移给幼稚的小鼠,并且寿命长。先前对肺部感染的免疫力在随后的疫苗接种和感染中显然起着重要且被低估的作用。该数据对某些患者组的疫苗接种时间具有重要意义,并且可能导致人类观察到的疾病易感性的差异。

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