Effective innate immune sensing is fundamental to host defence against viral infection. Influenza A virus (IAV) is a significant and persistent human respiratory pathogen that infects epithelial cells and macrophages along the respiratory tract. The prevailing dogma holds that macrophages sense intrinsic IAV infection through endosomal TLR7/8, which detect the ssRNA genome of incoming virions, and through cytosolic RIG-I, which senses 5’ triphosphate panhandle RNA structures present in the IAV genome or generated during IAV replication. However, our current understanding of IAV sensing in human macrophages is largely inferred from murine cells (e.g., dendritic cells, bone marrow-derived macrophages) or human epithelial cell lines, despite critical differences in viral life cycle, pattern recognition receptor expression, and ligand sensitivity between species and cell types. Here we map how primary human monocyte-derived macrophages sense IAV (pH1N1 Auck/09 and H3N2 SA/19) to drive potent antiviral and pro-inflammatory cytokine responses. Using a combination of pharmacological and genetic (CRISPR/Cas9 depletion) approaches, we find that human macrophages sense replicating IAV and that RIG-I drives early (6h) antiviral and pro-inflammatory cytokine responses. Unexpectedly, RIG-I is dispensable for IAV-induced antiviral responses at a late time point (24h) during infection. We uncover an alternative mode of RNA sensing that compensates for RIG-I loss during IAV infection, thereby driving ongoing antiviral cytokine release. Our findings challenge the current dogma of human macrophage IAV sensing and open new opportunities to target these pathways to augment or inhibit macrophage sensing and inflammatory responses during IAV infection.