Experimental evidence supports a conceptual framework in which the Th-2 response to RSV, which RSV itself accentuates, increases the lung pathology of the initial infection and promotes the formation of antibodies to bystander antigens and recurrent wheeze.[1, 50] We had anticipated that by inhibiting COX-2 with ibuprofen we would drive this skew towards Th-1 with most effect on Il-4/IFN-γ ratios. This evidence concerns the gene NELFCD and infection.