A novel influenza A virus mitochondrial protein that induces cell death
A novel influenza A virus mitochondrial protein that induces cell death
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DOI：
10.1038/nm1201-1306
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发表时间：
2001-12-01
期刊：
影响因子：
82.9
通讯作者：
Yewdell, JW
中科院分区：
文献类型：
--
作者：
Chen, WS;Calvo, PA;Yewdell, JW
在寻找可被CD 8（+）T细胞识别的甲型流感病毒编码的替代阅读框肽时，我们发现了由PB 1的+1阅读框编码的丰富的免疫原性肽。该肽来源于一种新的保守的87个残基的蛋白质，PB 1-F2，除了其翻译模式外，与其他流感基因产物相比，该蛋白质具有几个不寻常的特征。这些包括它在一些动物（特别是猪）流感病毒分离株中的缺失、个体感染细胞中的可变表达、快速蛋白酶体依赖性降解和线粒体定位。将细胞暴露于合成形式的PB 1-F2诱导细胞凋亡，并且具有干扰PB 1-F2表达的靶向突变的流感病毒在人单核细胞中诱导的细胞凋亡比具有完整PB 1-F2的那些更少。我们认为PB 1-F2的功能是杀死对流感病毒感染应答的宿主免疫细胞。
While searching for alternative reading-frame peptides encoded by influenza A virus that are recognized by CD8(+)T cells, we found an abundant immunogenic peptide encoded by the +1 reading frame of PB1. This peptide derives from a novel conserved 87-residue protein, PB1-F2, which has several unusual features compared with other influenza gene products in addition to its mode of translation. These include its absence from some animal (particularly swine) influenza virus Isolates, variable expression in individual infected cells, rapid proteasome-dependent degradation and mitochondrial localization. Exposure of cells to a synthetic version of PB1-F2 induces apoptosis, and influenza viruses with targeted mutations that interfere with PB1-F2 expression Induce less extensive apoptosis in human monocytic cells than those with intact PB1-F2. We propose that PB1-F2 functions to kill host immune cells responding to influenza virus infection.