Influenza A virus (IAV) is the primary cause of influenza, infecting up to a billion people annually and causing significant human and avian mortality. The virus is highly contagious and can evolve into highly pathogenic strains capable of human-to-human transmission, leading to pandemics. While antiviral drugs exist, they target only a few aspects of IAV replication and risk becoming obsolete due to resistance. This review aims to summarize the key steps in the IAV replication cycle and highlight areas of research that need more focus. The IAV genome consists of eight segmented, negative-sense, single-stranded RNA segments, each encoding several proteins essential for viral replication. The virus adopts either spherical or filamentous morphologies, with the latter being observed in lab-adapted strains. The viral envelope contains HA, NA, and M2 transmembrane proteins, while the matrix layer provides structural support. The viral genome is imported into the nucleus via the classical importin pathway, where the vRNP-resident polymerase transcribes viral mRNA and replicates the genome. The polymerase, composed of PB2, PB1, and PA, binds to the vRNA 3' and 5' termini and transcribes and replicates the genome. The HA protein mediates cell entry by binding to sialic acid, while the NA protein cleaves sialic acid from the viral surface. The M1 protein forms a helical filament that provides structural support, and the M2 protein facilitates viral membrane fusion and scission. The review also discusses the binding and endocytosis of IAV virions, the fusion of the viral and endosomal membranes, and the nuclear import of vRNPs. It highlights the importance of pH-dependent processes, such as virion acidification and viral-endosomal membrane fusion, in the replication cycle. The review emphasizes the need for further research to develop new antiviral strategies to combat the ongoing threat of IAV.Influenza A virus (IAV) is the primary cause of influenza, infecting up to a billion people annually and causing significant human and avian mortality. The virus is highly contagious and can evolve into highly pathogenic strains capable of human-to-human transmission, leading to pandemics. While antiviral drugs exist, they target only a few aspects of IAV replication and risk becoming obsolete due to resistance. This review aims to summarize the key steps in the IAV replication cycle and highlight areas of research that need more focus. The IAV genome consists of eight segmented, negative-sense, single-stranded RNA segments, each encoding several proteins essential for viral replication. The virus adopts either spherical or filamentous morphologies, with the latter being observed in lab-adapted strains. The viral envelope contains HA, NA, and M2 transmembrane proteins, while the matrix layer provides structural support. The viral genome is imported into the nucleus via the classical importin pathway, where the vRNP-resident polymerase transcribes viral mRNA and replicates the genome. The polymerase, composed of PB2, PB1, and PA, binds to the vRNA 3' and 5' termini and transcribes and replicates the genome. The HA protein mediates cell entry by binding to sialic acid, while the NA protein cleaves sialic acid from the viral surface. The M1 protein forms a helical filament that provides structural support, and the M2 protein facilitates viral membrane fusion and scission. The review also discusses the binding and endocytosis of IAV virions, the fusion of the viral and endosomal membranes, and the nuclear import of vRNPs. It highlights the importance of pH-dependent processes, such as virion acidification and viral-endosomal membrane fusion, in the replication cycle. The review emphasizes the need for further research to develop new antiviral strategies to combat the ongoing threat of IAV.