Herpes simplex virus (HSV) can infect a broad host range and cause mild to life threating infections in humans. The surface glycoproteins of HSV are evolutionarily conserved and show an extraordinary ability to bind more than one receptor on the host cell surface. Following attachment, the virus fuses its lipid envelope with the host cell membrane and releases its nucleocapsid along with tegument proteins into the cytosol. With the help of tegument proteins and host cell factors, the nucleocapsid is then docked into the nuclear pore. The viral double stranded DNA is then released into the host cell’s nucleus. Released viral DNA either replicates rapidly (more commonly in non-neuronal cells) or stays latent inside the nucleus (in sensory neurons). The fusion of the viral envelope with host cell membrane is a key step. Blocking this step can prevent entry of HSV into the host cell and the subsequent interactions that ultimately lead to production of viral progeny and cell death or latency. In this review, we have discussed viral entry mechanisms including the pH-independent as well as pH-dependent endocytic entry, cell to cell spread of HSV and use of viral glycoproteins as an antiviral target.

单纯疱疹病毒（HSV）可以感染广泛的宿主，并在人类中引起轻度甚至致命的感染。HSV的表面糖蛋白在进化上是保守的，显示出与宿主细胞表面上的多个受体结合的非凡能力。附着后，病毒将其脂质包膜与宿主细胞膜融合，并将其核衣壳和被膜蛋白释放到细胞质中。在外皮蛋白和宿主细胞因子的帮助下，核衣壳随后进入核孔。然后，病毒双链DNA被释放到宿主细胞的细胞核中。释放的病毒DNA可以快速复制（更常见于非神经元细胞中）或潜伏在细胞核内（在感觉神经元中）。病毒包膜与宿主细胞膜的融合是关键步骤。阻止此步骤可以防止HSV进入宿主细胞以及随后的相互作用，这些相互作用最终导致病毒后代的产生以及细胞死亡或潜伏期。在这篇综述中，我们讨论了病毒进入机制，包括pH依赖性和pH依赖性内吞进入，HSV的细胞间传播以及病毒糖蛋白作为抗病毒靶标的使用。