High viral load is associated with increased host responses. To be different with seasonal influenza virus, the H5N1 virus caused intense transcription induction and secretion of inflammatory cytokines/chemokines, as documented in human cases [15, 22] , and increased induction of cytokines and chemokines has been demonstrated in H5N1-infected mice [41] . Moreover, High virulence of H5N1 virus is associated with increase with increased host responses [42] . However, the relationship between viral load and host immuno-response has never been reported. Our study suggested that the high viral load is correlated with proinflamatory factors including IP-10, RANTES, MIP-3b and TRAIL. This finding is particularly relevant to the mechanism of H5N1 pathogenesis which is associated not only with the virus but also with the host responses. Inflammatory protein can be produced by almost any infected cells and by immune cells, including alveolar macrophages [43] . However, type II pneumocytes have a marked ability to secrete large amounts of cytokines, such as TNF-a, GM-CSF, MCP, and IL-8, in response to various insults [44, 45] and can be induced to secrete IL-1a, IL-6, RANTES, and MCP-1, in response to TNF-a [45, 46] , the last being produced by alveolar macrophages during H5N1 infection. Therefore, it is possible that the much greater cytokine induction by the H5N1 virus was as much a consequence of the response of individual, infected cells as it was a consequence of the numbers of infected cells.