Nucleotide sequences that affect replicative and transcriptional efficiencies of Sendai virus deletion mutants.
Structural features of the genomes of virus deletion mutants (DI virions) influence their replication efficiency. Among nonsegmented negative-strand RNA viruses, substitution of the genomic 3' terminus by a complementary copy of the 5' terminus (so-called "copy-back" sequence) could enhance replication either because the new 3' end is a better promoter of RNA replication or because DI RNAs that possess this sequence are incapable of acting as templates for transcription. Here we provide evidence that both mechanisms operate in mixed infections with Sendai virus DI RNAs. RNAs incapable of transcription always outgrew RNA species that were transcribed. This was true even when the 3'-terminal sequence of the untranscribed RNA was identical to the genomic 3' terminus, as in the case of an internally deleted DI genome (RNA Ra) rendered transcriptionally inert by point mutations of bases 47 and 51 at the 5' end of the positive-strand leader RNA template. Nevertheless, Ra was outgrown by a copy-back DI RNA, indicating that the 3' genomic end of Ra is a less efficient site for replication initiation than the copy-back sequence.
D001483:Base Sequence; D002872:Chromosome Deletion; D003673:Defective Viruses / Q000235:genetics / Q000502:physiology; D005814:Genes, Viral; D009154:Mutation; D010222:Parainfluenza Virus 1, Human / Q000235:genetics* / Q000502:physiology; D012367:RNA, Viral / Q000096:biosynthesis / Q000235:genetics*; D013698:Templates, Genetic; D014158:Transcription, Genetic; D014779:Virus Replication
D012367:RNA, Viral