Second-site mutations in Borna disease virus overexpressing viral accessory protein X.
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.
Department of Virology, University of Freiburg, D-79104 Freiburg, Germany.
Marion
M
Poenisch
Department of Virology, University of Freiburg, D-79104 Freiburg, Germany.
Sandra
S
Wille
Department of Virology, University of Freiburg, D-79104 Freiburg, Germany.
Urs
U
Schneider
Department of Virology, University of Freiburg, D-79104 Freiburg, Germany.
Peter
P
Staeheli
D000818:Animals; D001891:Borna disease virus / Q000235:genetics / Q000502:physiology*; D001921:Brain / Q000821:virology; D004252:DNA Mutational Analysis; D018628:Gene Dosage; D015967:Gene Expression Regulation, Viral; D055786:Gene Knockout Techniques; D020125:Mutation, Missense; D051381:Rats; D017422:Sequence Analysis, DNA; D054334:Viral Regulatory and Accessory Proteins / Q000096:biosynthesis* / Q000235:genetics*; D014779:Virus Replication
D054334:Viral Regulatory and Accessory Proteins