Ac23, an envelope fusion protein homolog in the Baculovirus Autographa califonica multicapsid nucleopolyhedrovirus, is a viral pathogenicity factor
Ac23, an envelope fusion protein homolog in the Baculovirus Autographa califonica multicapsid nucleopolyhedrovirus, is a viral pathogenicity factor
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DOI：
10.1128/jvi.77.1.328-339.2003
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发表时间：
2003-01-01
影响因子：
5.4
通讯作者：
Blissard, GW
中科院分区：
文献类型：
--
作者：
Lung, OY;Cruz-Alvarez, M;Blissard, GW
病毒包膜融合蛋白是介导病毒进入的重要结构蛋白，并且可以影响或决定病毒的宿主范围。这种包膜蛋白的获得、交换和进化可能会极大地影响病毒的成功和进化分歧。在Baculovitidae家族中，已经鉴定了两种非常不同的包膜融合蛋白。I组核型多角体病毒（NPV）如苜蓿银纹夜蛾多衣壳核型多角体病毒（AcMNPV）的出芽病毒体含有必需的GP 64包膜融合蛋白。相反，II组NPV和颗粒病毒没有gp64基因，而是编码一种称为F的不同包膜蛋白。来自II组NPVs的F蛋白可以在功能上替代gp64无效AcMNPV病毒中的GP64，表明GP64和这些F蛋白具有相似的功能作用。有趣的是，AcMNPV（和其他含gp64的I组NPV）也含有F基因同源物（Ac23），但AcMNPV F同源物不能补偿gp64的损失。在本研究中，我们表明，Ac23的表达，并发现在出芽的病毒粒子。为了研究含gp64的杆状病毒F蛋白同源物的功能，我们在E.杆菌我们发现，Ac23是不需要的病毒复制或致病细胞培养或感染的动物。但Ac23使受感染的昆虫宿主的死亡率提高了约28%或26 h。因此，Ac23代表了感染AcMNPV的幼虫中的重要病毒致病因子。
Viral envelope fusion proteins are important structural proteins that mediate viral entry and may affect or determine the host range of a virus. The acquisition, exchange, and evolution of such envelope proteins may dramatically affect the success and evolutionary divergence of viruses. In the family Baculovitidae, two very different envelope fusion proteins have been identified. Budded virions of group I nucleopolyhedroviruses (NPVs) such as the Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV), contain the essential GP64 envelope fusion protein. In contrast group II NPVs and granuloviruses have no gp64 gene but instead encode a different envelope protein called F. F proteins from group II NPVs can functionally substitute for GP64 in gp64null AcMNPV viruses, indicating that GP64 and these F proteins serve a similar functional role. Interestingly, AcMNPV (and other gp64-containing group I NPVs) also contain an F gene homolog (Ac23) but the AcMNPV F homolog cannot compensate for the loss of gp64. In the present study, we show that Ac23 is expressed and is found in budded virions. To examine the function of F protein homologs from the gp64-containing baculoviruses, we generated an Ac23null AcMNPV genome by homologous recombination in E. coli. We found that Ac23 was not required for viral replication or pathogenesis in cell culture or infected animals. However, Ac23 accelerated the mortality of infected insect hosts by approximately 28% or 26 h. Thus, Ac23 represents an important viral pathogenicity factor in larvae infected with AcMNPV.