Our study showed that IL-8 production obviously increased in HRV1B-infected HNECs at 72 h and was higher than IL-8 levels in HRV16-infected HNCEs, suggesting that upper respiratory infection symptoms (similar to asthma exacerbation) may be more severe in HRV1B infection than in HRV16 infection related to neutrophil burden [42]. This evidence concerns the gene CXCL8 and respiratory tract infectious disorder.