Incorporation of influenza A virus genome segments does not absolutely require wild-type sequences.
The efficient incorporation of influenza virus genome segments into virions is mediated by cis-acting regions at both ends of the viral RNAs. It was shown previously that nt 16-26 at the 3' end of the non-structural (NS) viral RNA of influenza A virus are important for efficient virion incorporation and that nt 27-56 also contribute to this process. To understand further the signalling requirements for genome packaging, this study performed linker-scanning mutagenesis in the latter region and found that nt 27-35 made an appreciable contribution to the efficient incorporation of the NS segment. An NS vRNA library was then generated composed of an RNA population with randomized nucleotides at positions 16-35 such that the virus could select the sequences it required for virion incorporation. The sequences selected differed from the wild-type sequence and no conserved nucleotides were selected. The ability of non-wild-type sequences to function in this manner indicates that the incorporation of influenza A virus genome segments does not absolutely require specific sequences.
Fujii
Ken
K
Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan.|Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Ozawa
Makoto
M
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI 53706, USA.|Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan.|Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Iwatsuki-Horimoto
Kiyoko
K
Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan.|Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Horimoto
Taisuke
T
Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan.|Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Kawaoka
Yoshihiro
Y
ERATO Infection-Induced Host Responses Project, Japan Science and Technology Agency, Saitama 332-0012, Japan.|Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan.|Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.|International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.|Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI 53706, USA.
D000818:Animals; D002460:Cell Line; D002522:Chlorocebus aethiops; D006801:Humans; D009980:Influenza A virus / Q000502:physiology*; D016254:Mutagenesis, Insertional / Q000379:methods; D012367:RNA, Viral / Q000235:genetics / Q000378:metabolism*; D019065:Virus Assembly
D012367:RNA, Viral