"Repair Me if You Can": Membrane Damage, Response, and Control from the Viral Perspective.
"Repair Me if You Can": Membrane Damage, Response, and Control from the Viral Perspective.
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DOI：
10.3390/cells9092042
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发表时间：
2020-09-07
期刊：
影响因子：
6
通讯作者：
Wodrich H
中科院分区：
文献类型：
--
作者：
Daussy CF;Wodrich H
细胞不断受到病原体（细菌、病毒和真菌）和蛋白质聚集体或化学物质的挑战，这些物质可在质膜或内-溶酶体隔室中引起膜损伤。内-溶酶体破裂的检测依赖于糖结合凝集素家族，称为半乳糖凝集素，其在膜损伤时感测聚糖异常暴露于细胞质。半乳糖凝集素与其他因子一起协调特异性膜损伤反应，例如招募转运所需的内体分选复合物（ESCRT）机制，以修复受损的膜或激活自噬以去除膜残留物。如果不加以控制，膜损伤会导致有害成分的释放，包括质子、活性氧或组织蛋白酶，从而引发炎症。在这篇综述中，我们提供了一个概述目前的知识膜损伤和细胞反应。特别是，我们专注于由无包膜病毒（如腺病毒）引发的内-溶酶体损伤，并讨论控制细胞膜损伤反应的病毒策略。最后，我们讨论了自噬与炎症之间的联系，并讨论了病毒进入后诱导自噬限制炎症的可能性。
Cells are constantly challenged by pathogens (bacteria, virus, and fungi), and protein aggregates or chemicals, which can provoke membrane damage at the plasma membrane or within the endo-lysosomal compartments. Detection of endo-lysosomal rupture depends on a family of sugar-binding lectins, known as galectins, which sense the abnormal exposure of glycans to the cytoplasm upon membrane damage. Galectins in conjunction with other factors orchestrate specific membrane damage responses such as the recruitment of the endosomal sorting complex required for transport (ESCRT) machinery to either repair damaged membranes or the activation of autophagy to remove membrane remnants. If not controlled, membrane damage causes the release of harmful components including protons, reactive oxygen species, or cathepsins that will elicit inflammation. In this review, we provide an overview of current knowledge on membrane damage and cellular responses. In particular, we focus on the endo-lysosomal damage triggered by non-enveloped viruses (such as adenovirus) and discuss viral strategies to control the cellular membrane damage response. Finally, we debate the link between autophagy and inflammation in this context and discuss the possibility that virus induced autophagy upon entry limits inflammation.
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