An increase of at least twice as many neutrophils (CD11b + , CD11c 2 , Ly6G/c + , CD4 2 , CD8-) was observed as early as 1 day p.i. in all infection groups, compared with neutrophils numbers in PBS-inoculated mice. On day 2 p.i. there was on average (n = 3 mice) over four hundred thousand more neutrophils in the lungs of 1918 virus inoculated mice than TX/91 inoculated mice. Significant differences in neutrophil populations (*p,0.05) between the HP and the LP virus groups emerged on day 3 p.i. and were sustained at each subsequent time point measured ( Figure 2B , b). On day 3 p.i., more than twice as many neutrophils were found in HP compared to LP infected lungs. Between days 3 and 7 p.i., lungs infected with HP viruses displayed a three fold increase in neutrophil numbers. At the peak of neutrophil infiltration on day 7 p.i, there was 4-8 million more neutrophils in the lungs of HP-infected animals compared to LP virus-infected mice. Although numbers of dendritic cells (CD11b 2 , CD11c + , Ly6G/c 2 , CD4 2 , CD8 2 ) ( Figure 2B , c) and CD4 + T (CD11b 2 , CD11c + , Ly6G/c 2 , CD8 2 ) and CD8 + T (CD11b 2 , CD11c + , Ly6G/c 2 , CD4 2 ) cells ( Figure 2B , d and e) in all groups of infected mice increased slightly compared with numbers in PBSinoculated animals during the course of infection, no significant differences were found between HP and LP infection groups, suggesting that these cell populations are not major contributors to the histopathological consolidation observed in lungs during HP H5N1 virus infections in mice [16] .