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. 1979 Dec;26(3):1009–1013. doi: 10.1128/iai.26.3.1009-1013.1979

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

G A Prince, S C Suffin, D A Prevar, E Camargo, D L Sly, W T London, R M Chanock
PMCID: PMC414720  PMID: 118925

Abstract

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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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