Phenotypic similarities and differences between UL37-deleted pseudorabies virus and herpes simplex virus type 1.
Phenotypic similarities and differences between UL37-deleted pseudorabies virus and herpes simplex virus type 1.
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UL37缺失的伪狂犬病病毒和1型单纯疱疹病毒表型的异同。
DOI：
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发表时间：
2009
影响因子：
3.8
通讯作者：
T. Mettenleiter
中科院分区：
文献类型：
--
作者：
Tobias Leege;H. Granzow;W. Fuchs;B. Klupp;T. Mettenleiter
在没有被膜蛋白pUL 37的情况下，伪狂犬病病毒（PrV）和单纯疱疹病毒1型（HSV-1）的病毒体形成严重受损。无包膜的核衣壳在细胞质中聚集成簇，而只有少数包膜颗粒可以检测到。虽然已经提出pUL 37对HSV-1的核出口的贡献，但在PrV-DeltaUL 37感染的细胞中，形态发生的核阶段没有受损。此外，HSV-1 pUL 37被描述为复制所必需的，而PrV能够在没有pUL 37的情况下有效地复制，尽管滴度低于野生型病毒。因此，各个pUL 37蛋白之间可能存在功能差异。本研究使用HSV-1毒株科斯的新型pUL 37缺失突变体HSV-1 DeltaUL 37，在平行试验中比较了UL 37缺失PrV和HSV-1的表型[86-1035]。在感染HSV-1 DeltaUL 37 [86-1035]或PrV-DeltaUL 37的非洲绿色猴（Vero）或兔肾（RK 13）细胞的细胞质中存在看似“裸露”的核衣壳聚集体。在两种病毒中均未观察到核衣壳的核保留。然而，与PrV-DeltaUL 37相反，HSV-1DeltaUL 37 [86-1035]不能在Vero或RK 13细胞中有效复制并在其上形成噬斑。相应缺失突变体与异源pUL 37的反式互补没有发生。这些数据表明HSV-1和PrV中保守的pUL 37具有相似但不同的功能。
In the absence of the tegument protein pUL37, virion formation of pseudorabies virus (PrV) and herpes simplex virus type 1 (HSV-1) is severely impaired. Non-enveloped nucleocapsids accumulate in clusters in the cytoplasm, whereas only a few enveloped particles can be detected. Although a contribution of pUL37 to nuclear egress of HSV-1 has been suggested, the nuclear stages of morphogenesis are not impaired in PrV-DeltaUL37-infected cells. Moreover, HSV-1 pUL37 has been described as essential for replication, whereas PrV is able to replicate productively without pUL37, although to lower titres than wild-type virus. Thus, there may be functional differences between the respective pUL37 proteins. This study compared the phenotypes of UL37-deleted PrV and HSV-1 in parallel assays, using a novel pUL37 deletion mutant of HSV-1 strain KOS, HSV-1DeltaUL37[86-1035]. Aggregates of seemingly 'naked' nucleocapsids were present in the cytoplasm of African green monkey (Vero) or rabbit kidney (RK13) cells infected with HSV-1DeltaUL37[86-1035] or PrV-DeltaUL37. Nuclear retention of nucleocapsids was not observed in either virus. However, in contrast to PrV-DeltaUL37, HSV-1DeltaUL37[86-1035] was unable to replicate productively in, and to form plaques on, either Vero or RK13 cells. Trans-complementation of respective deletion mutants with the heterologous pUL37 did not ensue. These data demonstrate that the conserved pUL37 in HSV-1 and PrV have similar but distinct functions.
影响因子：
3.7
作者：
Chen, DH;Jiang, H;Zhou, ZH
通讯作者：
Zhou, ZH
影响因子：
3.7
作者：
Lake, CM;Hutt-Fletcher, LM
通讯作者：
Hutt-Fletcher, LM