Influenza viruses are an important cause of respiratory infection worldwide. In humans, infection with seasonal influenza A virus (IAV) is generally restricted to the respiratory tract where productive infection of airway epithelial cells promotes viral amplification, dissemination, and disease. Alveolar macrophages (MΦ) are also among the first cells to detect and respond to IAV, where they play a pivotal role in mounting effective innate immune responses. In contrast to epithelial cells, IAV infection of MΦ is a "dead end" for most seasonal strains, where replication is abortive and newly synthesised virions are not released. Although the key replicative stages leading to productive IAV infection in epithelial cells are defined, there is limited knowledge about the abortive IAV life cycle in MΦ. In this review, we will explore host factors and viral elements that support the early stages (entry) through to the late stages (viral egress) of IAV replication in epithelial cells. Similarities, differences, and unknowns for each key stage of the IAV replicative cycle in MΦ will then be highlighted. Herein, we provide mechanistic insights into MΦ-specific control of seasonal IAV replication through abortive infection, which may in turn, contribute to effective host defence.

中文翻译：

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甲型流感病毒与巨噬细胞的相互作用：上皮细胞的教训。

流感病毒是全世界呼吸道感染的重要原因。在人类中，季节性A型流感病毒（IAV）的感染通常仅限于呼吸道，其中气道上皮细胞的生产性感染会促进病毒的扩增，传播和疾病。肺泡巨噬细胞（MΦ）也是最早检测和响应IAV的细胞之一，它们在启动有效先天免疫反应中起着关键作用。与上皮细胞相比，IAV感染MΦ是大多数季节性菌株的“死胡同”，在季节性菌株中复制是流产的，新合成的病毒粒子不会释放。尽管定义了导致上皮细胞中生产性IAV感染的关键复制阶段，但关于MΦ中IAV流产的生命周期知之甚少。在这篇评论中 我们将探讨支持IAV在上皮细胞复制的早期阶段（进入）到晚期阶段（病毒流出）的宿主因子和病毒成分。MΦ中IAV复制周期每个关键阶段的相似性，差异性和未知性将被突出显示。在此，我们提供了通过流产感染对MΦ特异性控制季节性IAV复制进行控制的机制，这可能反过来有助于有效的宿主防御。