West Nile virus (WNV) replication is independent of autophagy in mammalian cells.
West Nile virus (WNV) replication is independent of autophagy in mammalian cells.
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DOI：
10.1371/journal.pone.0045800
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Fredericksen BL
中科院分区：
文献类型：
--
作者：
Vandergaast R;Fredericksen BL
自噬是一个负责回收胞质蛋白和细胞器的稳态过程。此外，这一途径有助于细胞的内在先天防御。虽然许多病毒已经进化出对抗自噬途径的抗病毒作用的机制，但其他病毒破坏自噬以促进复制。在这里，我们研究了自噬在西尼罗河病毒（WNV）复制中的作用。来自各种来源的细胞系的实验，包括肾脏，肝脏，皮肤和大脑，表明WNV复制不上调自噬途径。此外，WNV感染并不抑制雷帕霉素诱导的自噬，表明WNV不破坏自噬信号级联。自噬途径的主要自噬因子Atg5或Atg7的耗尽扰动对WNV感染性颗粒的产生没有影响，表明WNV不需要功能性自噬途径进行复制。总之，我们的研究结果提供了证据表明，与黄病毒科的其他几种病毒不同，WNV不会与哺乳动物细胞中的常规自噬途径发生显着相互作用。
Autophagy is a homeostatic process responsible for recycling cytosolic proteins and organelles. Moreover, this pathway contributes to the cell’s intrinsic innate defenses. While many viruses have evolved mechanisms to antagonize the antiviral effects of the autophagy pathway, others subvert autophagy to facilitate replication. Here, we have investigated the role of autophagy in West Nile virus (WNV) replication. Experiments in cell lines derived from a variety of sources, including the kidney, liver, skin, and brain, indicated that WNV replication does not upregulate the autophagy pathway. Furthermore, WNV infection did not inhibit rapamycin-induced autophagy, suggesting that WNV does not disrupt the authophagy signaling cascade. Perturbation of the autophagy pathway by depletion of the major autophagy factors Atg5 or Atg7 had no effect on WNV infectious particle production, indicating that WNV does not require a functional autophagy pathway for replication. Taken together, the results of our study provide evidence that WNV, unlike several other viruses of the family Flaviviridae, does not significantly interact with the conventional autophagy pathway in mammalian cells.
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