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HIV血清阳性患者的血清抑制活性。

Serum suppressive activity of HIV seropositive patients.

作者信息

Israel-Biet D, Ekwalanga M, Venet A, Even P, Andrieu J M

机构信息

Hopital Laennec, Paris, France.

出版信息

Clin Exp Immunol. 1988 Nov;74(2):185-9.

Abstract

The mechanisms by which HIV induces immunosuppression are still poorly understood so far. Several pathways of CD4 cell destruction are known, including cytolysis with or without syncitium formation and killing by cytotoxic effectors of HIV infected or non-infected CD4 cells. However, a discrepancy exists between the small number of actually infected cells in vivo and the extent of HIV-related immunodeficiency. Among other possible immunosuppressive factors, serum blocking factors have been reported, but only in AIDS-related opportunistic infections (OI), i.e. in a quite specific type of full-blown HIV disease. The purpose of this work was to determine whether serum blocking activity was unique to this group of patients, or if it was also expressed in other clinical presentations and, moreover, at earlier stages of the disease. We also attempted to delineate the nature of these seric factors. In order to do so, we assessed serum suppressive activity of 50 HIV seropositive patients, seven with OI, eight with Kaposi's sarcoma (KS), and 35 with no clinical AIDS. Our results confirm the existence of serum inhibiting factors in AIDS, and demonstrate their presence at earlier stages of the disease. They also highlight the fact that the level of serum suppression does not correlate with patients clinical status, but increases with the severity of the disease. The lower the CD4 count, the higher the suppression exerted. Furthermore, we showed that the suppression was at least partly mediated by small size molecules, which are not complement-mediated or directly lymphocytotoxic. On the other hand, this activity does not correlate with the serum level of p24 HIV core protein. The possible relation with other viral components is discussed. The relevance of these data to prognosis and pathogenesis of HIV disease deserves further investigation.

摘要

迄今为止,人们对人类免疫缺陷病毒(HIV)诱导免疫抑制的机制仍知之甚少。已知有几种CD4细胞破坏途径,包括有或无融合体形成的细胞溶解以及HIV感染或未感染的CD4细胞的细胞毒性效应器杀伤。然而,体内实际感染细胞的数量与HIV相关免疫缺陷的程度之间存在差异。在其他可能的免疫抑制因素中,已报道了血清阻断因子,但仅在与艾滋病相关的机会性感染(OI)中,即在相当特定类型的晚期HIV疾病中。这项工作的目的是确定血清阻断活性是否是该组患者所特有的,或者它是否也在其他临床表现中表达,而且在疾病的早期阶段是否也有表达。我们还试图阐明这些血清因子的性质。为了做到这一点,我们评估了50名HIV血清阳性患者的血清抑制活性,其中7名患有OI,8名患有卡波西肉瘤(KS),35名无临床艾滋病症状。我们的结果证实了艾滋病中存在血清抑制因子,并证明它们在疾病的早期阶段就已存在。它们还突出了这样一个事实,即血清抑制水平与患者的临床状态无关,但随疾病严重程度的增加而升高。CD4细胞计数越低,抑制作用越强。此外,我们表明这种抑制至少部分是由小分子介导的,这些小分子不是补体介导的,也不是直接淋巴细胞毒性的。另一方面,这种活性与HIV核心蛋白p24的血清水平无关。讨论了与其他病毒成分的可能关系。这些数据与HIV疾病预后和发病机制的相关性值得进一步研究。

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