As observed for wholly human and avian influenza viruses, peak titers were reached for PR8+Vic HA/NA at both temperatures and PR8+Chick HA/NA at 37uC by 48 hrs pi after which a decline in viral titer was apparent. Again, as noted in our observations with human and avian influenza viruses, the loss of viral titers with time correlated with the onset of CPE. While PR8+Chick HA/NA infection at 32uC did not result in substantial AK release until 96 hr pi, increased AK activity was detected in cultures inoculated with this virus at 37uC. AK activity measured in cultures at this temperature increased with similar kinetics and reached similar levels as AK measured in cultures inoculated with PR8+Vic HA/NA at either temperature. Furthermore, the kinetics of AK induction demonstrated that again, AK was virus and (Cii) N1 reassortant virus. Data obtained in parallel for wild-type A/Victoria/3/75 is repeated in each graph (striped bars) for comparison to the mutant (solid bars). Data shown represents the mean of the percentage of influenza virus antigen-positive epithelium across 10 different fields +/ 2SE. Differences in viral antigen positive epithelium between temperatures for each virus at 48 hrs pi is noted as significant (*p,0.05) or insignificant (NS). A one-way ANOVA model showed no significant differences between the wild-type virus and PB2 mutant at 32uC and 37uC at 48 consequential to viral replication and that, overall, CPE induced by reassortant viruses was reflective of CPE measured for human and avian influenza viruses.