In the 1960s, the immunization of children with formalin inactivated-RSV (FI-RSV) vaccine not only failed to protect, but also yielded enhanced pulmonary disease in vaccinated infants following RSV infection (4, 5) . Studies with BALB/c mice have become a useful model for RSV pathogenesis, since FI-RSV-enhanced disease is also observed in vaccinated BALB/c mice. It is likely that the augmented lung disease and the development of pulmonary eosinophilia are attributed to an excessive Th2 type immune response (6) .