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感染致细胞病变的牛病毒性腹泻病毒的细胞中内源性凋亡途径的诱导

Induction of the intrinsic apoptotic pathway in cells infected with cytopathic bovine virus diarrhoea virus.

作者信息

Grummer B, Bendfeldt S, Wagner B, Greiser-Wilke I

机构信息

Institute of Virology, School of Veterinary Medicine, Buenteweg 17, 30559, Hannover, Germany.

出版信息

Virus Res. 2002 Dec;90(1-2):143-53. doi: 10.1016/s0168-1702(02)00150-8.

DOI:10.1016/s0168-1702(02)00150-8
PMID:12457970
Abstract

Cytopathic bovine viral diarrhoea virus (cp BVDV) induces apoptosis in bovine cell cultures. This also seems to be a prominent feature in the pathogenesis of mucosal disease. To gain an insight into the molecular pathways of the cell alterations, the involvement of different members of the apoptotic cascade was analyzed. It was shown that inhibition of the mitochondrial permeability transition pore significantly delayed the cytopathic effect without affecting virus replication. Moreover, the membrane potential (deltapsi(m)) was affected, and translocation of cytochrome c to the cytosol, overexpression of apoptotic protease-activating factor 1 and a significant increase of caspase-9 activity were demonstrated, indicating that the apoptosome is formed. We conclude that at least in vitro, infection of cells with cp BVDV leads to the activation of the intrinsic pathway of apoptosis.

摘要

细胞病变性牛病毒性腹泻病毒(cp BVDV)可在牛细胞培养物中诱导细胞凋亡。这似乎也是黏膜病发病机制中的一个显著特征。为深入了解细胞改变的分子途径,分析了凋亡级联反应不同成员的参与情况。结果表明,线粒体通透性转换孔的抑制显著延迟了细胞病变效应,而不影响病毒复制。此外,膜电位(Δψm)受到影响,细胞色素c转位至胞质溶胶,凋亡蛋白酶激活因子1过表达,且半胱天冬酶-9活性显著增加,表明凋亡小体形成。我们得出结论,至少在体外,cp BVDV感染细胞会导致内源性凋亡途径的激活。

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