Syndecan-1 and syndecan-2 play key roles in herpes simplex virus type-1 infection
Syndecan-1 and syndecan-2 play key roles in herpes simplex virus type-1 infection
复制标题
DOI：
10.1099/vir.0.027052-0
复制
发表时间：
2011-04-01
影响因子：
3.8
通讯作者：
Shukla, Deepak
中科院分区：
文献类型：
--
作者：
Bacsa, Sarolta;Karasneh, Ghadah;Shukla, Deepak
单纯疱疹病毒1型(HSV-1)是一种重要的人类病原体，也是发达国家传染性失明的主要原因。HSV-1利用硫酸乙酰肝素蛋白多糖(HSPG)附着在细胞上。虽然硫酸乙酰肝素(HS)部分在HSV-1感染中的重要性已经得到证实，但特定的蛋白多糖核心蛋白在感染过程中的作用仍然知之甚少。本研究的目的是评估Syndecan-1和Syndecan-2核心蛋白在HSV-1感染中的作用，这两种蛋白都在多种HSV-1靶细胞中表达。我们的结果表明，通过RNA干扰沉默syndecan-1和syndecan-2基因可以减少HSV-1的进入，减少空斑的形成，并促进细胞存活。此外，HSV-1感染增加了Syndecan-1和Syndecan-2蛋白的合成，从而增加了HS细胞表面的表达。我们的观察表明，Syndecan-1和Syndecan-2表达水平的变化可能与活动性病毒感染有关。综上所述，我们的发现为HSPG在HSV-1进入和传播过程中的作用提供了新的见解。
Herpes simplex virus type 1 (HSV-1) is an important human pathogen and a leading cause of infectious blindness in the developed world. HSV-1 exploits heparan sulfate proteoglycans (HSPG) for attachment to cells. While the significance of heparan sulphate (HS) moieties in HSV-1 infection is well established, the role of specific proteoglycan core proteins in the infection process remains poorly understood. The objective of this study was to assess the roles of syndecan-1 and syndecan-2 core proteins in HSV-1 infection, both of which are expressed by many HSV-1 target cell types. Our results demonstrate that syndecan-1 and syndecan-2 gene silencing by RNA interference reduces HSV-1 entry, plaque formation and facilitates cell survival. Furthermore, HSV-1 infection increases syndecan-1 and syndecan-2 protein synthesis and a resultant increase in cell surface expression of HS. Our observations suggest that changes in syndecan-1 and syndecan-2 expression levels may be related to active viral infection. Taken together, our findings provide new insights into HSPG functions during HSV-1 entry and spread.