Confer D L, Vercellotti G M, Kotasek D, Goodman J L, Ochoa A, Jacob H S
Department of Medicine, University of Minnesota, Minneapolis 55455.
Proc Natl Acad Sci U S A. 1990 May;87(9):3609-13. doi: 10.1073/pnas.87.9.3609.
Human endothelial cells or human foreskin fibroblasts infected with herpes simplex viruses (HSVs) potently inhibit the lytic activity of natural killer cells and interleukin 2-activated killer cells. The inhibition occurs after as little as 8 hr of viral infection and requires contact between effector cells and HSV-infected targets. Inhibition evidently stems from direct blockade of killer cell function because killer cells placed atop HSV-infected targets rapidly become incapable of lysing subsequently added HL-60 or K-562 cells. The impairment of killer cell function is prevented when protein glycosylation in HSV-infected cells is blocked with tunicamycin. These studies may be relevant for understanding the persistence of herpes simplex virus infections and, further, suggest a mechanism for failed immune surveillance.
感染单纯疱疹病毒（HSV）的人内皮细胞或人包皮成纤维细胞可有效抑制自然杀伤细胞和白细胞介素2激活的杀伤细胞的裂解活性。病毒感染仅8小时后就会出现这种抑制作用，并且需要效应细胞与感染HSV的靶细胞之间发生接触。抑制作用显然源于杀伤细胞功能的直接阻断，因为置于感染HSV的靶细胞之上的杀伤细胞会迅速丧失裂解随后添加的HL-60或K-562细胞的能力。当用衣霉素阻断感染HSV的细胞中的蛋白质糖基化时，杀伤细胞功能的损害就会得到预防。这些研究可能有助于理解单纯疱疹病毒感染的持续存在，并且进一步提示了免疫监视失败的一种机制。
