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- W2156875145 abstract "Borna disease virus (BDV) is a highly neurotropic virus that causes Borna disease, a virus-induced immune-mediated encephalomyelitis, in a variety of warm-blooded animals. Recent studies reported that BDV can be detected in patients with psychiatric disorders. BDV is noncytopathic, replicates in the nucleus of infected cells, and spreads intraaxonally in vivo. Upon infection of susceptible cultured cells, virus can be detected in foci. Little is known about the cellular components required for BDV replication. Here, we show that the cellular Raf/MEK/ERK signaling cascade is activated upon infection with BDV. In the presence of the MEK-specific inhibitor U0126, cells get infected with BDV; however, there is a block in virus spread to neighboring cells. The effect of the inhibitor on virus spread was still observed when the compound was added 2 h postinfection but not if treatment was initiated as late as 4 h after infection. Our results provide new insights into the BDV-host cell interaction and show that virus infection can be controlled with drugs interfering with a cellular signaling pathway. Since concentrations of the MEK inhibitor required to block BDV focus formation are not toxic for the host cells, our finding may be important with respect to antiviral drug development." @default.
- W2156875145 created "2016-06-24" @default.
- W2156875145 creator A5016200442 @default.
- W2156875145 creator A5042016744 @default.
- W2156875145 creator A5058408501 @default.
- W2156875145 date "2001-05-15" @default.
- W2156875145 modified "2023-10-18" @default.
- W2156875145 title "MEK-Specific Inhibitor U0126 Blocks Spread of Borna Disease Virus in Cultured Cells" @default.
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- W2156875145 doi "https://doi.org/10.1128/jvi.75.10.4871-4877.2001" @default.
- W2156875145 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/114241" @default.
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