Herpes simplex virus type-1 (HSV-1) and type-2 (HSV-2) are prototypical alphaherpesviruses that are characterized by their unique properties to infect trigeminal and dorsal root ganglionic neurons, respectively, and establish life-long latent infections. These viruses initially infect mucosal epithelial tissues and subsequently spread to neurons. They are associated with a significant disease spectrum, including orofacial and ocular infections for HSV-1 and genital and neonatal infections for HSV-2. Viral glycoproteins within the virion envelope bind to specific cellular receptors to mediate virus entry into cells. This is achieved by the fusion of the viral envelope with the plasma membrane. Similarly, viral glycoproteins expressed on cell surfaces mediate cell-to-cell fusion and facilitate virus spread. An interactive complex of viral glycoproteins gB, gD/gH/gL, and gK and other proteins mediate these membrane fusion phenomena with glycoprotein B (gB), the principal membrane fusogen. The requirement for the virion to enter neuronal axons suggests that the heterodimeric protein complex of gK and membrane protein UL20, found only in alphaherpesviruses, constitute a critical determinant for neuronal entry. This hypothesis was substantiated by the observation that a small deletion in the amino terminus of gK prevents entry into neuronal axons while allowing entry into other cells via endocytosis. Cellular receptors and receptor-mediated signaling synergize with the viral membrane fusion machinery to facilitate virus entry and intercellular spread. Unraveling the underlying interactions among viral glycoproteins, envelope proteins, and cellular receptors will provide new innovative approaches for antiviral therapy against herpesviruses and other neurotropic viruses.

中文翻译：

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每个故事都有两个方面：单纯疱疹病毒 1 型病毒糖蛋白 gB、gD、gH/gL、gK 和细胞受体在膜融合中发挥关键作用

单纯疱疹病毒 1 型 (HSV-1) 和 2 型 (HSV-2) 是典型的 alphaherpesviruses，其特征在于其独特的特性分别感染三叉神经和背根神经节神经元，并建立终身潜伏感染。这些病毒最初感染粘膜上皮组织，随后扩散到神经元。它们与重要的疾病谱相关，包括 HSV-1 的口面部和眼部感染以及 HSV-2 的生殖器和新生儿感染。病毒体包膜内的病毒糖蛋白与特定的细胞受体结合以介导病毒进入细胞。这是通过病毒包膜与质膜的融合来实现的。同样，在细胞表面表达的病毒糖蛋白介导细胞间融合并促进病毒传播。病毒糖蛋白 gB、gD/gH/gL 和 gK 和其他蛋白质的相互作用复合物与主要的膜融合原糖蛋白 B (gB) 介导这些膜融合现象。病毒粒子进入神经元轴突的要求表明，仅在 alphaherpesviruses 中发现的 gK 和膜蛋白 UL20 的异二聚体蛋白复合物构成了神经元进入的关键决定因素。观察到 gK 氨基末端的小缺失阻止进入神经元轴突，同时允许通过内吞作用进入其他细胞，这一假设得到了证实。细胞受体和受体介导的信号传导与病毒膜融合机制协同作用，以促进病毒进入和细胞间传播。揭示病毒糖蛋白、包膜蛋白、