Department of Biology, University of North Carolina at Charlotte, Charlotte, NC 28223, USA.
Virology. 2010 May 10;400(2):187-96. doi: 10.1016/j.virol.2010.01.025. Epub 2010 Feb 20.
Vesicular stomatitis virus (VSV) infection of mice via intranasal administration results in a severe encephalitis with rapid activation and proliferation of microglia and astrocytes. We have recently shown that these glial cells express RIG-I and MDA5, cytosolic pattern recognition receptors for viral RNA. However, it is unclear whether VSV can replicate in glial cells or if such replication is required for their inflammatory responses. Here we demonstrate that primary microglia and astrocytes are permissive for VSV infection and limited productive replication. Importantly, we show that viral replication is required for robust inflammatory mediator production by these cells. Finally, we have confirmed that in vivo VSV administration can result in viral infection of glial cells in situ. These results suggest that viral replication within resident glial cells might play an important role in CNS inflammation following infection with VSV and possibly other neurotropic nonsegmented negative-strand RNA viruses.
水疱性口炎病毒（VSV）经鼻腔感染小鼠会导致严重的脑炎，使小胶质细胞和星形胶质细胞迅速激活和增殖。我们最近发现这些神经胶质细胞表达 RIG-I 和 MDA5，这是细胞浆中识别病毒 RNA 的模式识别受体。然而，尚不清楚 VSV 是否可以在神经胶质细胞中复制，或者这种复制是否是其炎症反应所必需的。在这里，我们证明原代小胶质细胞和星形胶质细胞允许 VSV 感染和有限的有效复制。重要的是，我们表明病毒复制对于这些细胞产生丰富的炎症介质是必需的。最后，我们已经证实体内给予 VSV 可导致神经胶质细胞原位感染病毒。这些结果表明，在感染 VSV 及可能其他亲神经性非节段负链 RNA 病毒后，驻留神经胶质细胞内的病毒复制可能在中枢神经系统炎症中发挥重要作用。
