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Tick-borne encephalitis virus inhibits rRNA synthesis and host protein production in human cells of neural origin
M. Selinger, H. Tykalová, J. Štěrba, P. Věchtová, Z. Vavrušková, J. Lieskovská, A. Kohl, E. Schnettler, L. Grubhoffer,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
Grant support
MC_UU_12014/8
Medical Research Council - United Kingdom
NLK
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Public Library of Science (PLoS)
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from 2007-10-01
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from 2009-04-01
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from 2007
- MeSH
- Transcription, Genetic MeSH
- Encephalitis, Tick-Borne genetics metabolism virology MeSH
- Humans MeSH
- Cell Line, Tumor MeSH
- RNA Precursors MeSH
- Protein Biosynthesis genetics MeSH
- RNA, Ribosomal genetics metabolism MeSH
- RNA Polymerase I genetics metabolism MeSH
- Encephalitis Viruses, Tick-Borne physiology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Tick-borne encephalitis virus (TBEV), a member of the genus Flavivirus (Flaviviridae), is a causative agent of a severe neuroinfection. Recently, several flaviviruses have been shown to interact with host protein synthesis. In order to determine whether TBEV interacts with this host process in its natural target cells, we analysed de novo protein synthesis in a human cell line derived from cerebellar medulloblastoma (DAOY HTB-186). We observed a significant decrease in the rate of host protein synthesis, including the housekeeping genes HPRT1 and GAPDH and the known interferon-stimulated gene viperin. In addition, TBEV infection resulted in a specific decrease of RNA polymerase I (POLR1) transcripts, 18S and 28S rRNAs and their precursor, 45-47S pre-rRNA, but had no effect on the POLR3 transcribed 5S rRNA levels. To our knowledge, this is the first report of flavivirus-induced decrease of specifically POLR1 rRNA transcripts accompanied by host translational shut-off.
References provided by Crossref.org
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