Herpesvirus Interactions With Cell Surface Receptors

以前，我们发现单纯疱疹病毒1型（HSV-1）进入实验室细胞系的内吞作用，以及通过非内吞机制。HSV-1通过直接穿透质膜进入猴肾（Vero）细胞，而病毒通过pH依赖性内吞作用进入表达病毒进入受体的中国仓鼠卵巢（CHO）细胞。HSV-2通过粘膜表面或通过角质化鳞状上皮细胞的破裂感染人，然后传播到神经系统，在神经系统中病毒在神经元中建立潜伏期。我们已经发现HSV-1通过内吞作用进入原代和转化的表皮角质形成细胞，而病毒通过穿透质膜进入原代神经元和神经母细胞瘤细胞系。病毒进入角质形成细胞受到抑制内吞作用的试剂的抑制，例如升高内体pH或抑制细胞酪氨酸激酶活性的药物。这些相同的药物不能抑制病毒进入转化的神经元细胞。

Previously we discovered that herpes simplex type 1 (HSV-1) enters laboratory cell lines by endocytosis as well as by nonendocytosis mechanisms. HSV-1 enters monkey kidney (Vero) cells by direct penetration of the plasma membrane, while the virus enters Chinese hamster ovary (CHO) cells that express virus entry receptors by pH-dependent endocytosis. HSV-2 infects persons through mucosal surfaces or through breaks in keratinized squamous epithelial cells and then travels to the nervous system where the virus establishes latency in neurons. We have found that HSV-1 enters primary and transformed epidermal keratinocytes through endocytosis, while the virus enters primary neurons and neuroblastoma cell lines by penetration of the plasma membrane. Entry of the virus in keratinocytes is inhibited by agents that inhibit inhibit endocytosis such as drugs that elevate the pH of endosomes or inhibit cellular tyrosine kinase activity. These same drugs do not inhibit entry of the virus in transformed neuronal cells.