School of Biological Sciences, University of Queensland, St. Lucia, QLD, 4072, Australia.
Arch Virol. 2009;154(11):1737-43. doi: 10.1007/s00705-009-0512-8. Epub 2009 Sep 26.
Ascoviruses (AVs) are insect viruses transmitted by parasitoid wasps. The unique pathology in host cells upon AV infection includes enlargement, blebbing and cleavage of host cells into virus-containing vesicles that are important in dissemination of the virus. The mechanism of pathogenesis and vesicle formation is largely unknown. Here, we explored involvement of actin filaments in virus entry, replication and pathology. The results suggested that entry of Heliothis virescens ascovirus-3e (HvAV-3e) leads to rearrangement of the actin cytoskeleton. After HvAV-3e infection, actin filaments were found in foci rather than in a homogenous distribution within the cytoplasm. Actin filaments were also found concentrating around blebs and vesiculation areas of the cell cortex following infection. Destabilization of filamentous actin by cytochalasin D did not inhibit entry or replication of the virus but affected vesiculation and pathology associated with HvAV-3e infection. These observations suggested that actin may not be required for virus entry and replication but essential for virus pathology, mainly vesicle formation.
杆状病毒（AVs）是通过寄生蜂传播的昆虫病毒。在感染 AV 后，宿主细胞中独特的病理学包括宿主细胞的扩大、起泡和分裂成含有病毒的小泡，这对于病毒的传播很重要。发病机制和小泡形成的机制在很大程度上尚不清楚。在这里，我们探讨了肌动蛋白丝在病毒进入、复制和病理学中的作用。结果表明，Heliothis virescens ascovirus-3e（HvAV-3e）的进入导致肌动蛋白细胞骨架的重排。在 HvAV-3e 感染后，肌动蛋白丝在焦点中而不是在细胞质中均匀分布。在感染后，肌动蛋白丝也被发现在细胞皮层的泡状和囊泡化区域聚集。细胞松弛素 D 对丝状肌动蛋白的失稳不会抑制病毒的进入或复制，但会影响与 HvAV-3e 感染相关的囊泡化和病理学。这些观察结果表明，肌动蛋白可能不是病毒进入和复制所必需的，但对于病毒病理学，主要是囊泡形成是必不可少的。
