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Journal of Virology, October 2008, p. 9537-9545, Vol. 82, No. 19
0022-538X/08/$08.00+0     doi:10.1128/JVI.00639-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Polymerase Read-Through at the First Transcription Termination Site Contributes to Regulation of Borna Disease Virus Gene Expression {triangledown}

Marion Poenisch, Sandra Wille, Peter Staeheli,* and Urs Schneider*

Department of Virology, University of Freiburg, D-79104 Freiburg, Germany

Received 21 March 2008/ Accepted 15 July 2008

An unusually long noncoding sequence is located between the N gene of Borna disease virus (BDV) and the genes for regulatory factor X and polymerase cofactor P. Most of these nucleotides are transcribed and seem to control translation of the bicistronic X/P mRNA. We report here that Vero cells persistently infected with mutant viruses containing minor alterations in this control region showed almost normal levels of N, X, and P proteins but exhibited greatly reduced levels of mRNAs coding for these viral gene products. Surprisingly, cells infected with these BDV mutants accumulated a viral transcript 1.9 kb in length that represents a capped and polyadenylated mRNA containing the coding regions of the N, X, and P genes. Cells infected with wild-type BDV also contained substantial amounts of this read-through mRNA, which yielded both N and P protein when translated in vitro. Viruses carrying mutations that promoted read-through transcription at the first gene junction failed to replicate in the brain of adult rats. In the brains of newborn rats, these mutant viruses were able to replicate after acquiring second-site mutations in or near the termination signal located downstream of the N gene. Thus, sequence elements adjacent to the core termination signal seem to regulate the frequency by which the polymerase terminates transcription after the N gene. We conclude from these observations that BDV uses read-through transcription for fine-tuning the expression of the N, X, and P genes which, in turn, influence viral polymerase activity.

* Corresponding author. Mailing address: Department of Virology, University of Freiburg, Hermann-Herder-Strasse 11, D-79104 Freiburg, Germany. Phone for P. Staeheli: 49-761-203-6679. Fax: 49-761-203-5053. E-mail: peter.staeheli{at}uniklinik-freiburg.de. Phone for U. Schneider: 49-761-203-6222. Fax: 49-761-203-5053. E-mail: urs.schneider{at}uniklinik-freiburg.de

{triangledown} Published ahead of print on 23 July 2008.

Journal of Virology, October 2008, p. 9537-9545, Vol. 82, No. 19
0022-538X/08/$08.00+0     doi:10.1128/JVI.00639-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Poenisch, M., Wille, S., Schneider, U., Staeheli, P. (2009). Second-site mutations in Borna disease virus overexpressing viral accessory protein X. J. Gen. Virol. 90: 1932-1936 [Abstract] [Full Text]  
  • Rinder, M., Ackermann, A., Kempf, H., Kaspers, B., Korbel, R., Staeheli, P. (2009). Broad Tissue and Cell Tropism of Avian Bornavirus in Parrots with Proventricular Dilatation Disease. J. Virol. 83: 5401-5407 [Abstract] [Full Text]  
  • Poenisch, M., Burger, N., Staeheli, P., Bauer, G., Schneider, U. (2009). Protein X of Borna Disease Virus Inhibits Apoptosis and Promotes Viral Persistence in the Central Nervous Systems of Newborn-Infected Rats. J. Virol. 83: 4297-4307 [Abstract] [Full Text]  
  • Strawn, L. A., Lin, C. A., Tank, E. M.H., Osman, M. M., Simpson, S. A., True, H. L. (2009). Mutants of the Paf1 Complex Alter Phenotypic Expression of the Yeast Prion [PSI+]. Mol. Biol. Cell 20: 2229-2241 [Abstract] [Full Text]  


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