Influenza is an acute viral infection of the respiratory tract and there are many reports suggesting that many of the clinical and pathological manifestations of influenza virus are due to various cytokines. These proteins act as chemical messengers and aid in viral clearance and cell death, such as, interferon-a (IFN-α), Tumour Necrosis Factor-a (TNF-α), interleukin-1 (IL-1) α and β, interleukin-6 (IL-6), interleukin-8 (IL-8) and monocyte-attracting chemokines. Cytokine gene expression leads to activation of NF-?B, AP-1, STAT and IRF signal transducing molecules in influenza A virus-infected cells. Anti-viral defence mediated by influenza A virus-induced IFN-α/β have proved to be very essential. IFN-α/β is known to prolong T cell survival, upregulate IL-12 and IL-18 receptor gene expression and together with IL-18 stimulate NK and T cell IFN-γ production and the development of Th1-type immune response. It has been observed, though, not completely understood, that the cytokine responses differ depending on the type of host. This review aims to give a composed account of the cytokine/ chemokine responses, with special reference to the differences observed in various host-virus combinations.