Analysis of pseudorabies and herpes simplex virus recombinants simultaneously lacking the pUL17 and pUL25 components of the C-capsid specific component
Analysis of pseudorabies and herpes simplex virus recombinants simultaneously lacking the pUL17 and pUL25 components of the C-capsid specific component
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DOI：
10.1016/j.virusres.2010.06.022
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发表时间：
2010-10-01
期刊：
影响因子：
5
通讯作者：
Klupp, Barbara G.
中科院分区：
文献类型：
--
作者：
Kuhn, Jana;Leege, Tobias;Klupp, Barbara G.
单纯疱疹病毒1（HSV-1）的UL 17和UL 25基因产物的同源物在整个疱疹病毒科中是保守的，并且对于病毒复制是必需的。然而，它们的确切功能仍然未知。虽然这两种蛋白质在含有DNA的C-衣壳上形成复合物，但在不存在任何一种蛋白质的情况下观察到的缺陷不同。从HSV-1或相关的α疱疹病毒伪狂犬病病毒（Pry）中缺乏pUL 17排除了新复制的病毒DNA的切割和包装，而在缺乏pUL 25的情况下，基因组DNA被包裹，但衣壳向胞质溶胶的核出口被消除。HSV-1 pUL 25部分地补充了PrVUL 25缺失突变体中的缺陷，表明功能重叠。然而，相互互补并没有随之发生，本研究表明，UL 17缺失的HSV-1或Pry突变体也不能被异源pUL 17拯救。为了分析两种复合物配偶体的同时取代是否可以允许或增加反式互补，我们产生了共表达PrV或HSV-1 pUL 17和pUL 25以及各自的HSV-1和PrV双缺失突变体的兔肾细胞系。尽管两种双突变体的缺陷被共表达同源复合物配偶体的细胞系反式互补，但异源pUL 17和pUL 25不能恢复生产性复制。因此，PrV和HSV-1的蛋白质复合物要么具有不同的功能，要么需要与在异源环境中受损的其他病毒蛋白质相互作用。(C)2010 Elsevier B. V.保留所有权利。
Homologs of the UL17 and UL25 gene products of herpes simplex virus 1 (HSV-1) are conserved throughout the Herpesviridae and essential for virus replication. However, their exact function is still unknown. Although both proteins form a complex on DNA-containing C-capsids defects observed in the absence of either protein differ. Absence of pUL17 from HSV-1 or the related alphaherpesvirus pseudorabies virus (Pry) precludes cleavage and packaging of newly replicated viral DNA, whereas in the absence of pUL25 genomic DNA is encapsidated but nuclear egress of capsids to the cytosol is abolished. HSV-1 pUL25 partially complemented the defect in a PrVUL25 deletion mutant indicating overlapping functions. However, reciprocal complementation did not ensue, and the present study demonstrates that UL17-deleted HSV-1 or Pry mutants are also not rescued by heterologous pUL17. To analyze whether simultaneous substitution of both complex partners may allow or increase trans-complementation we generated rabbit kidney cell lines co-expressing either PrV or HSV-1 pUL17 and pUL25, and respective HSV-1 and PrV double deletion mutants. Whereas the defects of both double mutants were trans-complemented by cell lines co-expressing the homologous complex partners, productive replication was not restored by heterologous pUL17 and pUL25. Thus, the protein complexes of PrV and HSV-1 either possess distinct functions, or require interactions with other viral proteins which are impaired in a heterologous context. (C) 2010 Elsevier B.V. All rights reserved.