Enhanced polymerase activity confers replication competence of Borna disease virus in mice.
We previously showed that mouse adaptation of cDNA-derived Borna disease virus (BDV) strain He/80(FR) was associated exclusively with mutations in the viral polymerase complex. Interestingly, independent mouse adaptation of non-recombinant He/80 was correlated with different alterations in the polymerase and mutations in the viral glycoprotein. We used reverse genetics to demonstrate that changes in the polymerase which improve enzymatic activity represent the decisive host range mutations. The glycoprotein mutations did not confer replication competence in mice, although they slightly improved viral performance if combined with polymerase mutations. Our findings suggest that the viral polymerase restricts the host range of BDV.
Ackermann
Andreas
A
Department of Virology, University of Freiburg, D-79104 Freiburg, Germany.
Kugel
Daniela
D
Department of Virology, University of Freiburg, D-79104 Freiburg, Germany.
Schneider
Urs
U
Department of Virology, University of Freiburg, D-79104 Freiburg, Germany.
Staeheli
Peter
P
Department of Virology, University of Freiburg, D-79104 Freiburg, Germany.
D000818:Animals; D001890:Borna Disease / Q000401:mortality / Q000821:virology; D001891:Borna disease virus / Q000201:enzymology / Q000235:genetics* / Q000378:metabolism; D002460:Cell Line; D012321:DNA-Directed RNA Polymerases / Q000235:genetics* / Q000378:metabolism*; D051379:Mice; D009154:Mutation; D014764:Viral Proteins / Q000235:genetics / Q000378:metabolism; D014779:Virus Replication
D014764:Viral Proteins; D012321:DNA-Directed RNA Polymerases