Contribution of the leader sequence to homologous viral interference among Sendai virus strains.
Sendai viruses (SeV) derived from persistent infection have a capacity to interfere with co-infected wild-type virus. Here we showed that interference was also caused by the laboratory strains Z and Nagoya. The leader mutations A(20)U and A(24)U related to viral adaptation from mice to chicken eggs significantly affected the capacity for viral interference, especially through genome amplification. Furthermore, recombinant SeV that possessed the mutations A(34)G and G(47)A, which are commonly found in the leader sequence of persistent infection-derived SeV strains, had an increased capacity for interference. Viral replication of human parainfluenza viruses 1, 2, and 3, but not the mumps virus or Newcastle disease virus, was suppressed by co-infection of a persistent infection-derived SeV strain, suggesting suppression of closely related human paramyxoviruses. These results indicate that homologous interference is partly dependent on the promoter sequence and further suggest involvement of promoter activity for genome amplification related to host factors in viral interference.
Shimazu
Yukie
Y
Department of Virology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
Takao
Shin-Ich
SI
Irie
Takashi
T
Kiyotani
Katsuhiro
K
Yoshida
Tetsuya
T
Sakaguchi
Takemasa
T
D020121:5' Untranslated Regions / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001483:Base Sequence; D002460:Cell Line; D006224:Cricetinae; D006367:HeLa Cells; D006801:Humans; D008969:Molecular Sequence Data; D018098:Paramyxovirinae / Q000145:classification / Q000472:pathogenicity / Q000502:physiology; D029082:Sendai virus / Q000145:classification* / Q000235:genetics / Q000472:pathogenicity* / Q000502:physiology; D017422:Sequence Analysis, DNA; D014762:Viral Interference; D014779:Virus Replication
D020121:5' Untranslated Regions