To better understand potential influences on immune cell population dynamics in the lung following HP influenza virus infection as demonstrated in Figure 2B and Table 2 , we analyzed 17 chemokines and cytokines in the lungs of mice on days 1 and 4 p.i and report data here on 6 of the analytes that revealed significant differences among the viruses tested ( Figure 3 ). These earlier time points were chosen in an effort to understand the temporal relationship with lung immune cell infiltration in 1918 and Thai/16 infections ( Figure 2 ) and day 4 p.i. is a time when significant differences were observed in lung virus titers between HP and LP infection groups ( Figure 1 ). As shown in Figure 3 , on day 1 p.i. TX/91 infected lungs exhibited higher titers of IL-1a, IFN-c, and KC compared to 1918 virus-infected lungs though levels of MIP-1a, MCP-1, and IL-6 were higher in 1918 virus infected lungs. Cytokine levels were similar between the H5N1 viruses at day 1 p.i.. In contrast, lung tissue cytokine and chemokine levels at day 4 p.i. were higher among 1918 and Thai/ 16 virus-infected mice compared to those infected with the subtype-matched LP (TX/91 and SP/83) counterpart viruses for all cytokines and chemokines measured. Protein levels of the potent monocyte chemoattractant MCP-1 were 10-fold higher in 1918 and H5N1 virus-infected lungs than TX/91 virus-infected lungs, whereas levels of the MIP-1a chemokine were notably elevated in Thai/16 virus-infected lungs. KC (the mouse equivalent of human IL-8) [20, 23] levels were 10-fold higher in Thai/16 and 3-fold higher in 1918 virus infected lungs compared to TX/91 virus-infected lungs with SP/83 levels similar to 1918 infected lungs. The HP viruses were also potent inducers of IL-1a and IFNc. IL-6, (a generally pro-inflammatory cytokine) was also 