Sequential Changes in Cell-Mediated Immune Responses to Herpes Simplex Virus After Recurrent Herpetic Infection in Humans
Sequential Changes in Cell-Mediated Immune Responses to Herpes Simplex Virus After Recurrent Herpetic Infection in Humans
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人类复发性疱疹感染后细胞介导的单纯疱疹病毒免疫反应的连续变化
DOI：
10.1128/iai.18.1.130-137.1977
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发表时间：
1977
影响因子：
3.1
通讯作者：
T. Lehner
中科院分区：
文献类型：
--
作者：
E. Shillitoe;J. Wilton;T. Lehner
在 23 名复发性唇疱疹患者和 19 名对照受试者中研究了淋巴细胞对单纯疱疹病毒 (HSV) 的反应。血清阳性对照的淋巴细胞（而非血清阴性对照）通过掺入胸苷对HSV做出反应，并且上清液抑制豚鼠巨噬细胞的迁移。复发性疱疹病灶患者的淋巴细胞对 HSV 的反应是，与血清阳性对照相比，胸苷掺入显着增加，但上清液并未显示出增加的巨噬细胞迁移抑制反应。在病变发生后的 28 天内，HSV 的胸苷掺入量降至血清阳性对照的水平，然后上清液诱导巨噬细胞迁移的抑制增加。淋巴细胞对白色念珠菌、纯化蛋白衍生物或植物血凝素的反应不会根据病变的存在而波动，并且与对照组的反应没有差异。在血清阴性或血清阳性对照、有或无疱疹病变患者的血清存在下，淋巴细胞对 HSV 的反应不受培养的影响。这表明，在患有复发性唇疱疹的患者中，迁移抑制反应的周期性缺陷可能导致复发性感染的发生，并且体外HSV刺激的胸苷掺入增加是来自病变的抗原刺激的结果。
Lymphocyte responses to herpes simplex virus (HSV) were studied in 23 patients with recurrent herpes labialis and in 19 control subjects. Lymphocytes of seropositive, but not seronegative, controls responded to HSV by thymidine incorporation, and the supernatant fluids inhibited the migration of guinea pig macrophages. Lymphocytes from patients with a recurrent herpetic lesion responded to HSV by significantly greater thymidine incorporation than seropositive controls, but supernatants did not show an increased macrophage migration inhibition response. During the 28 days after the onset of a lesion, the thymidine incorporation to HSV fell to the level of the seropositive controls, and supernatants then induced an increased inhibition of macrophage migration. Lymphocyte responses to Candida albicans, purified protein derivative, or phytohemagglutinin did not fluctuate according to the presence of a lesion and did not differ from those of the controls. Lymphocyte responses to HSV were unaffected by culture in the presence of serum from seronegative or seropositive controls, or from patients with or without a herpetic lesion. It is suggested that in patients with recurrent herpes labialis a periodic defect of the migration inhibition response might have allowed the recurrent infection to develop, and that the increased thymidine incorporation stimulated by HSV in vitro is a result of antigenic stimulation from the lesion.