Inhibition of Theiler's virus-induced apoptosis in infected murine macrophages results in necroptosis.

Inhibition of Theiler's virus-induced apoptosis in infected murine macrophages results in necroptosis.
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DOI:
10.1016/j.virusres.2014.10.017
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发表时间:
2015-01-02
期刊:
影响因子:
5
通讯作者:
Lipton HL
Lipton HL
中科院分区:
医学3区
文献类型:
--
作者:
Son KN;Lipton HL

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在小鼠中,Theiler小鼠脑脊髓炎病毒(TMEV)持续存在于最终经历凋亡的巨噬细胞中。培养物中巨噬细胞的TMEV感染通过内在途径诱导细胞凋亡,限制病毒产量。我们发现,抑制TMEV诱导的细胞凋亡导致受体相互作用蛋白1(RIP1)的磷酸化,RIP1和RIP3的定位到线粒体,ROS的产生独立于MAPK激活和程序性坏死(坏死性凋亡)。阻断子宫内膜炎和坏死性凋亡都恢复了病毒产量。
In mice Theiler’s murine encephalomyelitis virus (TMEV) persists in macrophages that eventually undergo apoptosis. TMEV infection of macrophages in culture induces apoptosis through the intrinsic pathway, restricting virus yields. We show that inhibition of TMEV-induced apoptosis leads to phosphorylation of receptor interacting protein 1 (RIP1), localization of RIP1 and RIP3 to mitochondria, ROS production independent of MAPK activation and programmed necrosis (necroptosis). Blocking both apoptotis and necroptosis restored virus yields.
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