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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 sequences are well conserved in the virus family; nevertheless, they do exhibit some variations even within a virus species. In Sendai virus (SeV) Z strain, the E signals are identical for all six genes but there are four (N, P/M/HN, F, and L) different S signals with one or two nucleotide variations. The significance of these variations for in vitro and in vivo replication has been unknown. We addressed this issue by SeV reverse genetics. The luciferase gene was placed between the N and P gene so that recombinant SeVs expressed luciferase under the control of each of the four different S signals. The S signal for the F gene was found to drive a lower level of transcription than that of the other three, which exhibited comparable reinitiation capacities. The polar attenuation of SeV transcription thus appeared to be not linear but biphasic. Then, a mutant SeV whose F gene S signal was replaced with that used for the P, M, and HN genes was created, and its replication capability was examined. The mutant produced a larger amount of F protein and downstream gene-encoded proteins and replicated faster than wild-type SeV in cultured cells and in embryonated eggs. Compared with the wild type, the mutant virus also replicated faster in mice and was more virulent, requiring a dose 20 times lower to kill 50% of mice. On the other hand, the unique F start sequence as well as the other start sequences are perfectly conserved in all SeV isolates sequenced to date, including highly virulent fresh isolates as well as egg-adapted strains, with a virulence several magnitudes lower than that of the fresh isolates. This moderation of transcription at the F gene may therefore be relevant to viral fitness in nature.

* Corresponding author. Mailing address: Department of Viral Infection, Institute of Medical Science, University of Tokyo, Shirokanedai 4-6-1, 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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