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

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

Correspondence
Peter Staeheli
peter.staeheli{at}uniklinik-freiburg.de
Urs Schneider
urs.schneider{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.

Supplementary figures are available with the online version of this paper.