Respiratory syncytial virus (RSV) is one of the leading causes of viral respiratory tract infection in infants, the elderly and the immunocompromised worldwide, causing more deaths each year than influenza. Years of research into RSV since its discovery over 60 years ago have elucidated detailed mechanisms of the host-pathogen interface. RSV infection elicits widespread transcriptomic and proteomic changes, which both mediate the host innate and adaptive immune responses to infection, and reflect RSV's ability to circumvent the host stress responses, including stress granule formation, endoplasmic reticulum stress, oxidative stress, and programmed cell death. The combination of these events can severely impact on human lungs, resulting in airway remodeling and pathophysiology. The RSV membrane envelope glycoproteins (fusion F and attachment G), matrix (M) and nonstructural (NS) 1 and 2 proteins play key roles in modulating host cell functions to promote the infectious cycle. This review presents a comprehensive overview of how RSV impacts the host response to infection, and how detailed knowledge of the mechanisms thereof can inform the development of new approaches to develop RSV vaccines and therapeutics.

中文翻译：

---

呼吸道合胞病毒感染对宿主功能的影响：对抗病毒策略的影响。

呼吸道合胞病毒（RSV）是婴儿，老年人和全世界免疫功能低下病毒性呼吸道感染的主要原因之一，每年造成的死亡人数多于流感。自从60年前发现RSV以来，多年来的研究阐明了宿主-病原体界面的详细机制。RSV感染引起广泛的转录组和蛋白质组学变化，它们介导宿主对感染的先天性和适应性免疫反应，并反映RSV规避宿主应激反应的能力，包括应激颗粒形成，内质网应激，氧化应激和程序性细胞死亡。这些事件的结合会严重影响人的肺部，导致气道重塑和病理生理。RSV膜包膜糖蛋白（融合F和附着G），基质（M）和非结构性（NS）1和2蛋白在调节宿主细胞功能以促进感染周期中起关键作用。这篇综述全面概述了RSV如何影响宿主对感染的反应，以及有关其机理的详细知识如何可以为开发RSV疫苗和治疗剂的新方法提供信息。