title: Studies on mutation lesions and physiology of fowl plague virus ts mutants.
abstract: Temperature-sensitive (ts) mutants of fowl plague virus (FPV) were divided into six complementation groups. Experiments with ts mutants having defects of transcription showed that in FPV strain Weybridge, protein P1 coded by gene N2 takes part in primary transcription, and protein P3 coded for by gene N1 takes part in secondary transcription. Ts mutants of FPV with lower pathogenicity were present in all six complementation groups under study. Simultaneous inoculation of chickens with two pathogenic ts mutants of FPV caused death of the chickens and a pathogenic virus with ts+ phenotype was isolated from their organs. By recombination of ts multimutant FPV with human influenza virus a recombinant was obtained that contained genes coding for the haemagglutinin and neuraminidase of human influenza virus; all other genes were derived from FPV. In experiments on volunteers this recombinant appeared to be non-reactogenic but capable of inducing antibody formation.
mesh_terms: D000818:Animals; D002645:Chickens; D006389:Hemagglutinins, Viral / Q000235:genetics; D006801:Humans; D009980:Influenza A virus / Q000235:genetics* / Q000472:pathogenicity; D009154:Mutation; D014176:Protein Biosynthesis; D012367:RNA, Viral / Q000096:biosynthesis; D011995:Recombination, Genetic; D014158:Transcription, Genetic; D014611:Vaccination; D014779:Virus Replication
chemical_list: D006389:Hemagglutinins, Viral; D012367:RNA, Viral