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Journal of Virology, August 2002, p. 8244-8251, Vol. 76, No. 16
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.16.8244-8251.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

The Long Noncoding Region of the Human Parainfluenza Virus Type 1 F Gene Contributes to the Read-Through Transcription at the M-F Gene Junction

Tatiana Bousse,1 Tatyana Matrosovich,1,{dagger} Allen Portner,1,2 Atsushi Kato,3 Yoshiyuki Nagai,4 and Toru Takimoto1*

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, 38105,1 Department of Pathology, University of Tennessee, Memphis, Tennessee 38163,2 National Institute of Infectious Diseases, Musashimurayama, Tokyo 208-0011, Japan,3 Toyama Institute of Health, Toyama 939-0363, Japan4

Received 27 February 2002/ Accepted 10 May 2002

Sendai virus (SV) and human parainfluenza virus type 1 (hPIV1) have genomes consisting of nonsegmented negative-sense RNA in which the six genes are separated by well-conserved intergenic (IG) sequences and transcriptional start (S) and end signals. In hPIV1-infected cells, transcriptional termination at the M-F gene junction is ineffective; a large number of M-F read-through transcripts are produced (T. Bousse, T. Takimoto, K. G. Murti, and A. Portner, Virology 232:44-52, 1997). In contrast, few M-F read-through transcripts are detected in SV-infected cells. Sequence analysis indicated that the hPIV1 IG and S sequences in the M-F junction differ from those of SV. Furthermore, the hPIV1 F gene contains an unusually long noncoding sequence. To identify the cis-acting elements that prevent transcriptional termination at the M-F junction, we rescued recombinant SV (rSVhMFjCG) in which its M-F gene junction was replaced by that of hPIV1. Cells infected with rSVhMFjCG produced an abundance of M-F read-through transcripts; this result indicated that the hPIV1 M-F junction is responsible for inefficient termination. When one or both of the IG and S sites in rSVhMFjCG were replaced by those of SV, the efficiency of transcriptional termination increased but not to the level observed in wild-type SV-infected cells. Deletion of most of the long noncoding region of the hPIV1 F gene in rSVhMFjCG in addition to the mutations in IG and S signals resulted in efficient termination that was equivalent to the level observed in wild-type virus-infected cells. Therefore, the long noncoding sequence of the hPIV1 F gene contains cis-acting element(s) that affects transcriptional termination. Our evaluation of the effect of inefficient transcriptional termination on viral replication in culture revealed that cells infected with rSVhMFjCG produced less F protein than cells infected with wild-type SV and that assembly of the recombinant SV in culture was less efficient. These phenotypes seem to be responsible for the extended survival of mice infected with rSVhMFjCG.

* Corresponding author. Mailing address: Department of Infectious Diseases, Mail Stop 330, St. Jude Children's Research Hospital, 332 N. Lauderdale, Memphis, TN 38105-2794. Phone: (901) 495-3375. Fax: (901) 523-2622. E-mail: toru.takimoto{at}stjude.org.

{dagger} Present address: Institut fur Virologie, Philipps-Universitat, 35037 Marburg, Germany.

Journal of Virology, August 2002, p. 8244-8251, Vol. 76, No. 16
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.16.8244-8251.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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