Influenza A virus (IAV) is a major respiratory pathogen causing seasonal epidemics and pandemics, posing serious threats to public health and livestock. The high mutation rate of IAV leads to vaccine mismatches and drug-resistant variants, underscoring the need for novel antiviral strategies. This review examines the role of lactylation in IAV-host interactions, focusing on three core questions: how IAV induces lactylation, how lactylation reshapes antiviral immunity, and how IAV exploits lactylation for immune evasion. Key findings include lactylation of viral vRNP components required for efficient replication and the host deacetylase SIRT1, which suppresses IAV replication by removing these lactyl groups. IAV counteracts this defense by downregulating SIRT1 expression. Lactylation also regulates cGAS-STING, RLR-MAVS, and IFN signaling pathways. The therapeutic potential of targeting lactate metabolism and SIRT1 is discussed. Understanding lactylation in IAV infection may open new avenues for antiviral drug development.