There is abundant evidence that the innate immune response to influenza A virus (IAV) is highly complex and plays a key role in protection against IAV induced infection and illness. Unfortunately it also clear that aspects of innate immunity can lead to severe morbidity or mortality from IAV, including inflammatory lung injury, bacterial superinfection, and exacerbation of reactive airways disease. We review broadly the virus and host factors that result in adverse outcomes from IAV and show evidence that inflammatory responses can become damaging even apart from changes in viral replication per se, with special focus on the positive and adverse effects of neutrophils and monocytes. We then evaluate in detail the role of soluble innate inhibitors including surfactant protein D and antimicrobial peptides that have a potential dual capacity for down-regulating viral replication and also inhibiting excessive inflammatory responses and how these innate host factors could possibly be harnessed to treat IAV infection. Where appropriate we draw comparisons and contrasts the SARS-CoV viruses and IAV in an effort to point out where the extensive knowledge existing regarding severe IAV infection could help guide research into severe COVID 19 illness or vice versa.

有大量证据表明，对甲型流感病毒（IAV）的先天免疫应答非常复杂，并且在预防IAV引起的感染和疾病中起关键作用。不幸的是，这也清楚地表明，先天免疫的各个方面都可能导致IAV的严重发病或死亡，包括炎症性肺损伤，细菌过度感染和反应性气道疾病的加重。我们广泛地审查了导致IAV不良结果的病毒和宿主因素，并显示出炎症反应甚至会破坏病毒复制的变化，从而证明炎症反应会变得有害本身，特别关注中性粒细胞和单核细胞的正面和负面影响。然后，我们详细评估可溶性先天性抑制剂的作用，包括表面活性剂蛋白D和抗菌肽，它们具有潜在的双重能力，可下调病毒复制并抑制过度的炎症反应，以及如何利用这些先天宿主因子来治疗IAV感染。在适当的情况下，我们进行比较和对比SARS-CoV病毒和IAV，以指出在哪里存在有关严重IAV感染的广泛知识可以帮助指导对严重COVID 19疾病的研究，反之亦然。