There appears to be wide disparity in results concerning extrapulmonary spread of avian H5N1 viruses and pathology in animal models. In mice, virus has been recovered from most extrapulmonary tissues examined, including brain, but viral titers were often low and inconsistent [8] [9] [10] . In cynomolgus macaques infected with the H5N1 virus-strain A/Hong Kong/156/97, virus replication was mainly confined to the respiratory tract [11, 12] . In contrast, in cats infected with H5N1-strain A/Vietnam/1194/2004, high titers of virus were re-isolated from most extrapulmonary tissues and organs regardless of infection route [13] . Similar results were obtained in ferrets with the virus strain A/Hong Kong/486/97, despite the latter strains having relatively low pathogenicity in mice [8, 10, 14] . These species differences may reflect variations in virus receptor distribution [15] , variations in inflammatory and immune responses [16] [17] [18] [19] , or differences inherent to the H5N1 strains used, such as replication efficiency in host cells, interference with interferon responses [8, 10, 20, 21] , or any combination of these variables.