Respiratory syncytial virus infection in owl monkeys: viral shedding, immunological response, and associated illness caused by wild-type virus and two temperature-sensitive mutants.
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.
D000818:Animals; D000914:Antibodies, Viral / Q000032:analysis*; D001029:Aotus trivirgatus; D000882:Haplorhini; D009154:Mutation; D009305:Nasopharynx / Q000382:microbiology; D009500:Neutralization Tests; D012136:Respiratory Syncytial Viruses / Q000276:immunology / Q000302:isolation & purification*; D012141:Respiratory Tract Infections / Q000276:immunology / Q000382:microbiology*; D010253:Respirovirus Infections / Q000276:immunology / Q000382:microbiology*; D013696:Temperature
D000914:Antibodies, Viral