2003年12月
Transfection of prion protein gene suppresses coxsackievirus B3 replication in prion protein gene-deficient cells
JOURNAL OF GENERAL VIROLOGY
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- 巻
- 84
- 号
- 開始ページ
- 3495
- 終了ページ
- 3502
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1099/vir.0.19222-0
- 出版者・発行元
- SOC GENERAL MICROBIOLOGY
The susceptibility of prion protein gene (Prnp)-null cells to coxsackievirus B3 (CVB3) was investigated. Primary cultures of murine Prnp(-/-) brain cells were more sensitive to CVBs than corresponding cells from wild-type mice. The viral susceptibility of a Prnp-null cell line (HpL3-4) derived from the murine hippocampus was compared with that of two established cell lines (HeLa. and HEp-2) that are widely employed for CVB3 studies. After infection with CVB3, HpL3-4 cells showed a very rapid and complete cytopathic effect (CPE). CPE developed earlier and viruses replicated at higher titres in HpL3-4 cells compared with HeLa and HEp-2 cells. Under a semi-solid medium, plaques developed rapidly in CVB3-infected HpL3-4 cells. To confirm the effect of Prnp on virus infection, a Prnp(-/-) cell line and a Prnp-transfected neuronal cell line were analysed. The replication and release of infectious particles of CVB3 in Prnp(-/-) cells were significantly more effective than those of the Prnp-transfected cell line. Levels of type I interferon (IFN) after CVB3 infection were higher in the Prnp-transfected cell line than in Prnp(-/-) cells, whereas apoptotic cells were more obvious in the Prnp(-/-) cells than in those of the Prnp-transfected cell line. These findings suggest that the absence of Prnp retards the induction of CVB3-induced IFNs, resulting in an enhanced CVB3 production and apoptotic cell death. Furthermore, our data indicate that the HpL3-4 cell line may provide a novel and sensitive system for isolation of CVB3 from clinical specimens.
- リンク情報
- ID情報
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- DOI : 10.1099/vir.0.19222-0
- ISSN : 0022-1317
- Web of Science ID : WOS:000220465300032