Abstract: Objective To investigate the apoptosis mechanism of respiratory syncytial virus (RSV) and provide a new way of clinical therapy through the change of NF-κB after RSV infected A549 and IMR-90 cell. Methods RSV with the multiplicity of infection (MOI) 3 infecting A549 and IMR-90 cell, cell morphological change was observed using optical microscope, cell viability was detected with MTT, RSV viral titer was detected using empty spot test. Caspase-3, 8, 9 、cytochrome-c and NF-κB protein expression were detected using western - blot method. Results RSV infection A549 and IMR - 90 cell, A549 cell survival was lower than IMR - 90, intracellular virus titer was higher than IMR – 90 (P < 0.05). Cell showed obviously apoptosis change. Caspase-3, 8, 9 and cytochrome-c in time-dependence increased. Caspase-9 expressions were observed. In early (< 8h)RSV infection NF-κB was activated in time dependent manner, 8h to the peak, 24h began to decline. NF-κB expression was down-regulated after 36h RSV infection (P < 0.01). Conclusion RSV can through the endogenous and exogenous way caused A549 cell apoptosis. The endogenous way was primary. NF-κB played a certain role in the process.

Key words: RSV、NF-κB、apoptosis