Background: Influenza A virus displays morphological heterogeneity, existing as both spherical and filamentous particles. While viral morphology has long been observed, its role in pathogenesis, replication efficiency and immune evasion remains underexplored. Therefore, this research aims to compare spherical and filamentous influenza variants in terms of replication dynamics, inhibitor resistance, and cell-to-cell spread. Methods: Using plasmid-based reverse genetics, we generated a toolbox of fluorescently tagged influenza A viruses with site-specific M1 mutations or M-gene swaps to induce spherical or filamentous phenotypes. Viral replication and morphology were assessed through single- and multi-cycle growth curves, plaque assays and microscopy. Neutralisation, exit and entry inhibitor assays (using anti-HA antibodies, neuraminidase inhibitors, macropinocytosis inhibitors and endocytosis inhibitors) were performed to quantify morphology-specific viral resistance. Results: Inducing a filamentous morphology in a normally spherical virus background resulted in a higher replication efficiency in the absence of any inhibitors in both single- and multi-cycle growth curves. We also observed that filamentous viruses were more resistant than spherical viruses to endocytosis inhibitors and neutralisation by anti-HA antibodies; however, both spherical and filamentous viruses were inhibited by a neuraminidase inhibitor. In contrast, the addition of a macropinocytosis inhibitor only neutralised the filamentous virus. Fluorescence microscopy was used to gain insights into the effects of viral morphology on cell-to-cell spread. Conclusion: We have demonstrated that viral morphology has a significant impact on influenza replication kinetics. These findings highlight morphology as an underappreciated determinant of influenza virus fitness.