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10.1099/vir.0.011841-0

http://scihub22266oqcxt.onion/10.1099/vir.0.011841-0
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19420156!ä!19420156

suck abstract from ncbi


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pmid19420156      J+Gen+Virol 2009 ; 90 (Pt 8): 1932-1936
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  • Second-site mutations in Borna disease virus overexpressing viral accessory protein X #MMPMID19420156
  • Poenisch M; Wille S; Schneider U; Staeheli P
  • J Gen Virol 2009[Aug]; 90 (Pt 8): 1932-1936 PMID19420156show ga
  • 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.
  • |*Gene Dosage[MESH]
  • |*Gene Expression Regulation, Viral[MESH]
  • |*Mutation, Missense[MESH]
  • |Animals[MESH]
  • |Borna disease virus/genetics/*physiology[MESH]
  • |Brain/virology[MESH]
  • |DNA Mutational Analysis[MESH]
  • |Gene Knockout Techniques[MESH]
  • |Rats[MESH]
  • |Sequence Analysis, DNA[MESH]
  • |Viral Regulatory and Accessory Proteins/*biosynthesis/*genetics[MESH]


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