HAE cultures infected with A/Victoria/3/75 at either 32uC or 37uC and A/Dk/Eng/62 at 37uC viewed en face exhibited loss of integrity of the epithelium although the extent of injury and time of onset varied ( Figure 2A ). Further evaluation of histological cross-sections indicated that A/Victoria/3/75 infection at 37uC, which had the highest and earliest induction of AK, resulted in the earliest evidence of morphological injury at 72 hrs pi. HAE infected with A/Victoria/3/75 at 32uC or 37uC or A/Dk/Eng/62 at 37uC all showed desquamation of the superficial layer of columnar epithelial cells with basal epithelial cells remaining attached to the matrix support by 120 hrs pi ( Figure 2B ). Similar cytopathology has been reported for A/Udorn/307/72 influenza virus infection of HAE in vitro and for clinical human influenza virus infection in vivo [29, 33] . The detection of AK in apical washes of A/Dk/Eng/62-infected HAE at 32uC suggested that this virus did eventually compromise cellular integrity at the lower temperature, but dramatic morphological effects were not seen at least for up to 120 hrs ( Figure 1B and 2B). It should be noted, however, that at 120 hrs pi, A/Dk/Eng/62-infected HAE at 32uC did display some morphological characteristics different from uninfected and infected HAE at earlier time-points. Preliminary assessment indicates that expansion of lateral spaces between the columnar epithelial cells had occurred. Although we do not know the significance of these morphological changes, we speculate these observations are the initiation of CPE that will ultimately result in similar cellular injury as seen for this virus at 37uC and human viruses at both temperatures.