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鸡胚成纤维细胞对传染性法氏囊病病毒感染的凋亡反应反映了病毒的致病性。

Apoptotic response of chicken embryonic fibroblast cells to infectious bursal disease virus infections reflects viral pathogenicity.

作者信息

Shahsavandi Shahla, Ebrahimi Mohammad Majid, Sadeghi Kaveh, Mahravani Homayoon

机构信息

Razi Vaccine and Serum Research Institute, PO box 31975-148, Karaj, Iran,

出版信息

In Vitro Cell Dev Biol Anim. 2014 Oct;50(9):858-64. doi: 10.1007/s11626-014-9783-9. Epub 2014 Jul 4.

DOI:10.1007/s11626-014-9783-9
PMID:24993162
Abstract

Infectious bursal disease virus (IBDV) induces immunodeficiency in young chickens and apoptosis in chicken embryos. To understand the relation between the viral pathogenesis and the induction of cell death, chicken embryonic fibroblast (CEF) cells were infected with IBDV intermediate (im) and very virulent (vv) strains at different MOIs. The cell viability and DNA fragmentation were evaluated in infected cells. The cellular apoptotic pathway involve was investigated by determining the activities of caspase cascade. The imIBDV strain was replicated well in CEF cells and shown higher viral titers than vvIBDV. Apoptosis changes were observed only in vvIBDV-infected CEF cells at higher MOI 48 h post infection. Efflux of cytochrome c suggests that the intrinsic pathway of the apoptotic process induced by vvIBDV infection independently of virus replication. Prediction of caspase substrates cleavage sites revealed that different IBDV strains have conserved cleavage motif pattern for VP2 and VP5 viral proteins. These findings suggest the pathogenicity of IBDV strains might be involved in the induction of apoptosis in host cells.

摘要

传染性法氏囊病病毒(IBDV)可导致幼鸡免疫缺陷,并在鸡胚中诱导细胞凋亡。为了解病毒致病机制与细胞死亡诱导之间的关系,用不同感染复数(MOI)的IBDV中等毒力(im)株和超强毒力(vv)株感染鸡胚成纤维细胞(CEF)。对感染细胞的细胞活力和DNA片段化进行评估。通过测定半胱天冬酶级联反应的活性来研究细胞凋亡途径。imIBDV株在CEF细胞中复制良好,且病毒滴度高于vvIBDV。感染48小时后,仅在MOI较高的vvIBDV感染的CEF细胞中观察到凋亡变化。细胞色素c的外流表明,vvIBDV感染诱导的凋亡过程的内在途径独立于病毒复制。对半胱天冬酶底物切割位点的预测表明,不同的IBDV株对VP2和VP5病毒蛋白具有保守的切割基序模式。这些发现表明,IBDV株的致病性可能与宿主细胞凋亡的诱导有关。

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本文引用的文献

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PLoS One. 2014 Jan 9;9(1):e84503. doi: 10.1371/journal.pone.0084503. eCollection 2014.
2
Fas/FasL and perforin-granzyme pathways mediated T cell cytotoxic responses in infectious bursal disease virus infected chickens.Fas/FasL和穿孔素-颗粒酶途径介导传染性法氏囊病病毒感染鸡的T细胞细胞毒性反应。
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3
A single amino acid V4I substitution in VP1 attenuates virulence of very virulent infectious bursal disease virus (vvIBDV) in SPF chickens and increases replication in CEF cells.
传染性法氏囊病病毒感染细胞在干扰素α作用下细胞凋亡加剧。
J Virol. 2018 May 14;92(11). doi: 10.1128/JVI.00364-18. Print 2018 Jun 1.
4
VP2 of Infectious Bursal Disease Virus Induces Apoptosis via Triggering Oral Cancer Overexpressed 1 (ORAOV1) Protein Degradation.传染性法氏囊病病毒的VP2通过触发口腔癌过表达蛋白1(ORAOV1)降解诱导细胞凋亡。
Front Microbiol. 2017 Jul 19;8:1351. doi: 10.3389/fmicb.2017.01351. eCollection 2017.
5
Infectious Bursal Disease Virus-Host Interactions: Multifunctional Viral Proteins that Perform Multiple and Differing Jobs.传染性法氏囊病病毒与宿主的相互作用:执行多种不同功能的多功能病毒蛋白
Int J Mol Sci. 2017 Jan 14;18(1):161. doi: 10.3390/ijms18010161.
VP1 中的单个氨基酸 V4I 取代可减弱超强毒传染性法氏囊病病毒(vvIBDV)在 SPF 鸡中的毒力,并增加在 CEF 细胞中的复制。
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