Sendai Virus Gene Start Signals Are Not Equivalent in Reinitiation Capacity: Moderation at the Fusion Protein Gene

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Journal of Virology, November 1999, p. 9237-9246, Vol. 73, No. 11
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Sendai Virus Gene Start Signals Are Not Equivalent in Reinitiation Capacity: Moderation at the Fusion Protein Gene

Atsushi Kato,¹^,² Katsuhiro Kiyotani,³ Mohammad K. Hasan,¹ Tatsuo Shioda,⁴ Yuko Sakai,¹ Tetsuya Yoshida,³ and Yoshiyuki Nagai¹^,⁵^,^*

Department of Viral Infection¹ and Department of Infectious Diseases,⁴ Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Department of Viral Diseases and Vaccine Control² and AIDS Research Center,⁵ National Institute of Infectious Diseases, Tokyo 208-0011, and Department of Bacteriology, Hiroshima University School of Medicine, Hiroshima 734-8551,³ Japan

Received 11 May 1999/Accepted 9 August 1999

In paramyxovirus transcription, viral RNA polymerase synthesizes each monocistronic mRNA by recognizing the gene start (S)and end (E) signals flanking each gene. These signal sequencesare well conserved in the virus family; nevertheless, they doexhibit some variations even within a virus species. In Sendaivirus (SeV) Z strain, the E signals are identical for all sixgenes but there are four (N, P/M/HN, F, and L) different S signalswith one or two nucleotide variations. The significance of thesevariations for in vitro and in vivo replication has been unknown.We addressed this issue by SeV reverse genetics. The luciferasegene was placed between the N and P gene so that recombinant SeVsexpressed luciferase under the control of each of the four differentS signals. The S signal for the F gene was found to drive a lowerlevel of transcription than that of the other three, which exhibitedcomparable reinitiation capacities. The polar attenuation of SeVtranscription thus appeared to be not linear but biphasic. Then,a mutant SeV whose F gene S signal was replaced with that usedfor the P, M, and HN genes was created, and its replication capabilitywas examined. The mutant produced a larger amount of F proteinand downstream gene-encoded proteins and replicated faster thanwild-type SeV in cultured cells and in embryonated eggs. Comparedwith the wild type, the mutant virus also replicated faster inmice and was more virulent, requiring a dose 20 times lower tokill 50% of mice. On the other hand, the unique F start sequenceas well as the other start sequences are perfectly conserved inall SeV isolates sequenced to date, including highly virulentfresh isolates as well as egg-adapted strains, with a virulenceseveral magnitudes lower than that of the fresh isolates. Thismoderation of transcription at the F gene may therefore be relevantto viral fitness innature.

^* Corresponding author. Mailing address: Department of Viral Infection, Institute of Medical Science, University of Tokyo, Shirokanedai4-6-1, Minato-ku, Tokyo 108-8639, Japan. Phone: 81-3-5449-5285.Fax: 81-3-5449-5409. E-mail: ynagai{at}ims.u-tokyo.ac.jp.

Journal of Virology, November 1999, p. 9237-9246, Vol. 73, No. 11
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

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