HSV-1 ICP0: paving the way for viral replication.

HSV-1 ICP0: paving the way for viral replication.
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DOI:
10.2217/fvl.11.24
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发表时间:
2011-04
期刊:
影响因子:
3.1
通讯作者:
Davido DJ
Davido DJ
中科院分区:
医学4区
文献类型:
--
作者:
Smith MC;Boutell C;Davido DJ

文献摘要

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单纯疱疹病毒1型(HSV-1)的病毒生命周期有两个不同的阶段:裂解和潜伏。一种负责决定生产性裂解复制和从潜伏期再激活之间的平衡的病毒立即早期蛋白是感染细胞蛋白0(ICP 0)。ICP 0是一种含有775个氨基酸的真正有趣的新基因(RING)指蛋白,其具有E3泛素连接酶活性,其是ICP 0激活HSV-1基因表达、破坏核结构域(ND)10结构、介导细胞蛋白降解以及逃避宿主细胞的内在和先天抗病毒防御所必需的。本文探讨了我们目前对ICP 0的反式激活,E3泛素连接酶,抗宿主防御活动及其相互关系的理解。最后,我们将讨论ICP 0的这些特性如何被用作HSV-1抗病毒治疗的可能靶点。
Herpes simplex virus type 1 (HSV-1) has two distinct phases of its viral life cycle: lytic and latent. One viral immediate-early protein that is responsible for determining the balance between productive lytic replication and reactivation from latency is infected cell protein 0 (ICP0). ICP0 is a 775-amino acid really interesting new gene (RING)-finger-containing protein that possesses E3 ubiquitin ligase activity, which is required for ICP0 to activate HSV-1 gene expression, disrupt nuclear domain (ND) 10 structures, mediate the degradation of cellular proteins, and evade the host cell’s intrinsic and innate antiviral defenses. This article examines our current understanding of ICP0’s transactivating, E3 ubiquitin ligase, and antihost defense activities and their inter-relationships to one another. Lastly, we will discuss how these properties of ICP0 may be utilized as possible targets for HSV-1 antiviral therapies.