Viral bronchiolitis is the single most common cause of hospitalization of infants in the western world, but the development of effective preventative or therapeutic stratagems has been hampered by lack of information about its pathogenesis. The majority of cases are caused by respiratory syncytial virus (RSV), the annual hospitalization costs of which were estimated to be $300 million in 1988 in the United States alone, with 91,000 children admitted (1). Antiviral immunity appears not only to protect against infection but also to contribute to lung pathology. The first evidence that specific immunity could be harmful came in the 1960s, when children were vaccinated with formalin-inactivated RSV. Vaccine recipients developed strong serologic responses but were not protected against infection. Most vaccinees who subsequently became infected with RSV developed severe lower respiratory tract disease, and some died as a result. The reasons for vaccine-augmented disease have been studied (2-5), but no safe, effective vaccine has yet been produced. RSV belongs to the genus pneumovirus in the family Paramyxoviridae, bearing close similarity to measles, canine distemper virus, mumps, and parainfluenza viruses. Electron microscopy shows irregularly shaped and often clumped virions with a lipid envelope bearing the surface glycoproteins G, F, and SH. The nucleocapsid contains a single-strand negative sense RNA genome of 5 x 106 kD, which is nonsegmented. There are ten genes, with 12 potential gene products. Sequential transcription occurs from 3'to 5'; the first genes to be transcribed are ic and Ib, which encode nonstructural proteins of unknown function. Then fol-