获得性免疫缺陷综合征(AIDS)患者和AIDS高危人群中的修饰核苷:与淋巴和免疫参数的相关性

A Fischbein, J G Bekesi, S Solomon, E Borek, O K Sharma
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引用次数: 0

摘要

患有某些恶性疾病的患者在其尿液中排泄的修饰核苷水平升高,主要源于转移RNA (tRNA)的分解。获得性免疫缺陷综合征(艾滋病)通常与进展迅速的卡波西肉瘤(KS)有关,目前在许多国家都有发生。男同性恋者被认为是患这些疾病的风险最高的。我们以前报道过艾滋病患者分泌修饰核苷水平升高。在这篇通讯中,我们报告了77名在检查时没有艾滋病临床表现的男同性恋者的改良核苷水平。在这一高危人群中发现异常核苷水平的频率很高。在被认为是艾滋病前驱症状的淋巴结肿大患者中,有较高水平的趋势。在一些核苷(假尿嘧啶和二甲基鸟苷)和淋巴结肿大程度之间发现了统计学上显著的相关性。假尿嘧啶、1-甲基腺苷和二甲基鸟苷与总t淋巴细胞百分比(T11)、抑瘤性t淋巴细胞百分比(T8)和自然杀伤细胞数量(Leu-7)呈负相关。这些发现表明,尿核苷水平的测定可能有助于识别艾滋病高危人群。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Modified nucleosides in patients with acquired immune deficiency syndrome (AIDS) and individuals at high risk of AIDS: correlations with lymphadenomegaly and immunological parameters.

Patients with certain malignant diseases excrete in their urine elevated levels of modified nucleosides originating predominantly from the breakdown of transfer RNA (tRNA). Acquired immune deficiency syndrome (AIDS), often associated with rapidly progressing Kaposi's sarcoma (KS), is currently occurring in many countries. Male homosexuals are considered to be at highest risk of developing these disorders. We have previously reported that patients with AIDS excrete elevated levels of modified nucleosides. In this communication, we report on modified nucleoside levels measured in 77 male homosexuals without clinical manifestations of AIDS at the time of examination. A high frequency of abnormal nucleoside levels was found in this high-risk group. There was a trend towards higher levels in individuals with lymphadenomegaly, considered a prodrome of AIDS. Statistically significant correlations were found between some of the nucleosides (pseudouridine and dimethylguanosine) and degree of lymphadenomegaly. Pseudouridine, 1-methyl-adenosine and dimethylguanosine were inversely related to percentages of total T-lymphocytes (T11), suppressor T-lymphocytes (T8), and number of natural killer cells (Leu-7). These findings suggest that determination of urinary nucleoside levels may help identify individuals at high risk of developing AIDS.

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