Protection of mice from wild-type Sendai virus infection by a trypsin-resistant mutant, TR-2.
A trypsin-resistant mutant of Sendai virus, TR-2, which could be activated by chymotrypsin but not by trypsin or the protease present in mouse lung, was inoculated intranasally into mice after being activated in vitro. TR-2 hardly brought about clinical illness or lung lesions in mice; the protease present in the lung could not activate the progeny virus, and the infection terminated after one-step replication. Nevertheless, the immunoglobulin A antibody against wild-type Sendai virus was produced in the respiratory tracts as well as the serum immunoglobulin G antibody, and the mice were protected from the challenge of the wild-type Sendai virus. On the basis of these results, TR-2 may provide a new model of live vaccine for paramyxoviruses; its availability as a live vaccine is also discussed.
Tashiro
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Homma
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D000818:Animals; D002460:Cell Line; D002522:Chlorocebus aethiops; D004352:Drug Resistance, Microbial; D007668:Kidney; D008168:Lung / Q000382:microbiology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009154:Mutation; D009500:Neutralization Tests; D010222:Parainfluenza Virus 1, Human / Q000187:drug effects / Q000254:growth & development* / Q000472:pathogenicity; D018184:Paramyxoviridae Infections / Q000382:microbiology*; D014357:Trypsin / Q000494:pharmacology*; D014775:Virus Activation
D014357:Trypsin