Mechanism of HSV infection through soluble adapter-mediated virus bridging to the EGF receptor.
Mechanism of HSV infection through soluble adapter-mediated virus bridging to the EGF receptor.
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DOI：
10.1016/j.virol.2011.02.014
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发表时间：
2011-04-25
期刊：
影响因子：
3.7
通讯作者：
Glorioso JC
中科院分区：
文献类型：
--
作者：
Nakano K;Kobayashi M;Nakamura K;Nakanishi T;Asano R;Kumagai I;Tahara H;Kuwano M;Cohen JB;Glorioso JC
单纯疱疹病毒进入细胞需要包膜糖蛋白D（gD）与进入受体结合。根据细胞的不同，进入通过不同的机制发生，包括在细胞表面的融合或内吞作用。在这里，我们研究了进入机制，通过非HSV受体介导的可溶性双特异性衔接蛋白组成的识别元件gD和EGF受体（EGFR）。病毒使用EGF或EGFR特异性单链抗体（scFv）进入内体用于受体识别。使用EGF衔接子的感染效率较低，这可能归因于其与病毒gD的结合较弱。由scFv衔接子介导的感染是pH敏感的，表明单独的gD-EGFR桥接不足以从内体释放衣壳。我们还表明，scFv衔接子增强了体内EGFR表达肿瘤组织的感染。我们的研究结果表明，适配器可以重新定位HSV感染，而不会彻底改变进入机制。
Herpes simplex virus entry into cells requires the binding of envelope glycoprotein D (gD) to an entry receptor. Depending on the cell, entry occurs by different mechanisms, including fusion at the cell surface or endocytosis. Here we examined the entry mechanism through a non-HSV receptor mediated by a soluble bi-specific adapter protein composed of recognition elements for gD and the EGF receptor (EGFR). Virus entered into endosomes using either EGF or an EGFR-specific single chain antibody (scFv) for receptor recognition. Infection was less efficient with the EGF adapter which could be attributed to its weaker binding to viral gD. Infection mediated by the scFv adapter was pH sensitive, indicating that gD-EGFR bridging alone was insufficient for capsid release from endosomes. We also show that the scFv adapter enhanced infection of EGFR-expressing tumor tissue in vivo. Our results indicate that adapters may retarget HSV infection without drastically changing the entry mechanism.
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