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Intranasal inoculation of owl monkeys with wild-type respiratory syncytial virus induced upper respiratory tract disease in each of seven animals. The response of owl monkeys to two highly defective, temperature-sensitive, multiple-lesion mutants was then compared to the pattern seen with wild-type respiratory syncytial virus. These mutants, ts-1 NG-1 and ts-1 NG-16, were derived from the ts-1 mutant that had been remutagenized with nitrosoguanidine (NG). Previously the ts-1 NG-1 and ts-1 NG-16 mutants had been shown to be more temperature sensitive and more stable genetically than their ts-1 parent. Both ts-1 NG-1 and ts-1 NG-16 produced infection that was delayed in onsent compared to wild-type virus infection. However, the mutants were shed from the upper respiratory tract for the same period of time and at the same titer as wild-type virus. The serum neutralizing antibody response to infection with the mutants was nearly equivalent to that elicited by wild-type virus. However, the extent of disease induced by the mutants was significantly less than that seen with wild-type virus. These observations suggest that the mutants are potential vaccine condidates and should be subjected to additional in vivo testing in primates and, ultimately, humans.

infection and immunity

Respiratory syncytial virus infection in owl monkeys: viral shedding, immunological response, and associated illness caused by wild-type virus and two temperature-sensitive mutants