Influenza viruses are enveloped, single-stranded, negative-sense RNA viruses belonging to the Orthomyxoviridae family. Infections with influenza A viruses (IAV), classified based on hemagglutinin (HA) and neuraminidase glycoproteins, represent a significant global health issue with an annual estimate of 1 billion cases and 250–500 000 deaths worldwide [1].

IAV infections pose a formidable challenge to the host, which needs to mount effective defence and repair responses while avoiding excessive lung inflammation and damage associated with severe hypoxemia and acute respiratory distress syndrome (ARDS) 2, 3, 4•, 5•. Indeed, in order to allow efficient gas diffusion and support life, the airways must be permeable, and the air–blood barrier must remain very thin. Hence, the lung immune system has evolved as a sophisticated surveillance and defence system to sustain physiological functions and host protection. Dedicated to these tasks, distinct populations of monocytes and resident tissue macrophages (ResMacs) populate the steady-state lung (Box 1). Upon IAV infection, additional monocytes and monocyte-derived Macs (Mo-Macs) are recruited and undergo a dynamic response postinfection, which unfolds with remarkable complexity 6, 7. In this article, we aim to review the journey of monocytes and macrophages during and after IAV infection, thus unravelling the intricacies of their roles in viral clearance, inflammation, tissue repair, immunomodulation, and tissue imprinting (Figure 1).