Influenza remains a significant social threat especially regarding the emergence of new mutant or reassortant strains. Measures of prophylaxis do not provide complete and stable protection from infection and the use of antivirals results in high-level occurrence of resistant forms of viruses. Nowadays more and more attention is paid to find new targets for antiviral therapy that are not directly connected with virus proteins but can act indirectly through cellular mechanisms involved in viral replication. This approach requires complete understanding of various cellular pathways used by influenza virus. Here we present a brief overview of interactions between influenza A virus and the cell cytoskeleton. This interaction is initiated from the very beginning of influenza infection--adsorption--and continues with endocytosis, release of viral RNP and its entry into the nucleus. The role of cytoskeleton during the late stages of infection is also of great importance. It takes part in NP translocation from the nucleus to the cytoplasm, virus assembly and budding. The presence of cellular actin in certain influenza virions is therefore not accidental but reflects the peculiarities of interaction between a virus and a host cell.