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This Article Full Text (Papers in Press[PDF]) All Versions of this Article: vir.0.011841-0v1 90/8/1932    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Poenisch, M. Articles by Staeheli, P. Search for Related Content PubMed PubMed Citation Articles by Poenisch, M. Articles by Staeheli, P. Agricola Articles by Poenisch, M. Articles by Staeheli, P.

Second-site mutations in Borna disease virus overexpressing viral accessory protein X

University of Freiburg

¹ E-mail: peter.staeheli{at}uniklinik-freiburg.de

The X protein of Borna disease virus (BDV) is an essential factor that regulates viral polymerase activity and inhibits apoptosis of persistently infected cells. We observed that a BDV mutant which carries an additional X gene replicated well in cell culture only after acquiring second-site mutations that selectively reduced expression of the endogenous X gene. In rat brains, the virus acquired additional mutations which inactivated the ectopic X gene or altered the sequence of X. These results demonstrate that BDV readily acquires mutations if strong selection pressure is applied. They further indicate that fine-tuning of X expression determines viral fitness.

Received 13 March 2009; accepted 6 May 2009.