Parainfluenza virus 5 genomes are located in viral cytoplasmic bodies whilst the virus dismantles the interferon-induced antiviral state of cells.
Parainfluenza virus 5 genomes are located in viral cytoplasmic bodies whilst the virus dismantles the interferon-induced antiviral state of cells.
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DOI：
10.1099/vir.0.012047-0
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发表时间：
2009-09
期刊：
影响因子：
--
通讯作者：
Randall RE
中科院分区：
文献类型：
--
作者：
Carlos TS;Young DF;Schneider M;Simas JP;Randall RE
尽管最初在干扰素（IFN）诱导的抗病毒状态的细胞中严重损害了Parainfluenza病毒的复制周期（PIV5），但该病毒仍然针对STAT1降级。 24-48小时后，它们从抗病毒状态中脱离，在IFN诱导的抗病毒状态下感染细胞后，建立了正常的病毒。最初，使用NP和L基因特异的问题，这些细胞质体在小细胞质体内，这些细胞质体的出现与感染细胞的STAT1丧失相关细胞质体与应力颗粒，细胞质p-bodies或自噬小体的细胞标记不会共定位。病毒蛋白和/或核蛋白质的聚集物可以简单地被“冷震”活细胞分散，这一过程破坏了细胞骨架，鉴于在体内感染期间，抗病毒状态，我们建议这些细胞质体是PIV5基因组驻留的区域，而病毒会消除细胞的抗病毒状态。在PIV5绕过IFN系统的策略中起着重要的作用。
Although the replication cycle of parainfluenza virus type 5 (PIV5) is initially severely impaired in cells in an interferon (IFN)-induced antiviral state, the virus still targets STAT1 for degradation. As a consequence, the cells can no longer respond to IFN and after 24−48 h, they go out of the antiviral state and normal virus replication is established. Following infection of cells in an IFN-induced antiviral state, viral nucleocapsid proteins are initially localized within small cytoplasmic bodies, and appearance of these cytoplasmic bodies correlates with the loss of STAT1 from infected cells. In situ hybridization, using probes specific for the NP and L genes, demonstrated the presence of virus genomes within these cytoplasmic bodies. These viral cytoplasmic bodies do not co-localize with cellular markers for stress granules, cytoplasmic P-bodies or autophagosomes. Furthermore, they are not large insoluble aggregates of viral proteins and/or nucleocapsids, as they can simply and easily be dispersed by ‘cold-shocking’ live cells, a process that disrupts the cytoskeleton. Given that during in vivo infections, PIV5 will inevitably infect cells in an IFN-induced antiviral state, we suggest that these cytoplasmic bodies are areas in which PIV5 genomes reside whilst the virus dismantles the antiviral state of the cells. Consequently, viral cytoplasmic bodies may play an important part in the strategy that PIV5 uses to circumvent the IFN system.
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