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预测HIV-1血清阳性者患艾滋病及生存情况的免疫激活标志物。

Immune activation markers to predict AIDS and survival in HIV-1 seropositives.

作者信息

Fuchs D, Jäger H, Popescu M, Reibnegger G, Werner E R, Dierich M P, Kaboth W, Tilz G P, Wachter H

机构信息

Institute of Medical Chemistry and Biochemistry, University of Innsbruck, Austria.

出版信息

Immunol Lett. 1990 Oct;26(1):75-9. doi: 10.1016/0165-2478(90)90178-s.

DOI:10.1016/0165-2478(90)90178-s
PMID:2125976
Abstract

Neopterin concentrations in body fluids of HIV-1 seropositives provide predictive information. In 1986, we examined serum and urine neopterin concentrations in 29 HIV-1 seropositives. Serum levels of soluble IL-2 receptor (sIL2R), soluble CD8 (sCD8), tumour necrosis factor alpha (TNF-alpha) and circulating immune complexes (CIC) were retrospectively analysed in 1989. All individuals had increased serum and urine neopterin, sIL2R and CIC concentrations, 27/29 had increased sCD8 concentrations, whereas all had normal TNF-alpha levels. During a 3-year follow-up, high urine and serum neopterin concentrations were significantly associated with progression to AIDS and with the occurrence of AIDS-associated death. Both neopterin variables were of similar predictive value (p less than 0.001, generalized Wilcoxon test). sIL2R concentrations were of borderline significance in predicting the onset of AIDS (p = 0.05). All other parameters lacked predictive information in our study. We conclude, that chronic immune activation is detectable in almost all HIV-1 seropositives. Chronic immune activation may be associated with HIV-1 replication and may contribute to the immunopathology of HIV-1 infection.

摘要

HIV-1血清阳性者体液中的新蝶呤浓度可提供预测信息。1986年,我们检测了29例HIV-1血清阳性者的血清和尿液新蝶呤浓度。1989年对可溶性白细胞介素-2受体(sIL2R)、可溶性CD8(sCD8)、肿瘤坏死因子α(TNF-α)和循环免疫复合物(CIC)的血清水平进行了回顾性分析。所有个体的血清和尿液新蝶呤、sIL2R和CIC浓度均升高,27/29的个体sCD8浓度升高,而所有个体的TNF-α水平均正常。在3年的随访期间,高尿液和血清新蝶呤浓度与进展为艾滋病及艾滋病相关死亡的发生显著相关。两个新蝶呤变量具有相似的预测价值(p<0.001,广义Wilcoxon检验)。sIL2R浓度在预测艾滋病发病方面具有临界显著性(p = 0.05)。在我们的研究中,所有其他参数均缺乏预测信息。我们得出结论,几乎所有HIV-1血清阳性者均可检测到慢性免疫激活。慢性免疫激活可能与HIV-1复制有关,并可能导致HIV-1感染的免疫病理学改变。

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