包奇州HIV感染者血浆分泌钙调蛋白水平的研究

A. Musab, Ibrahim Yazid Gobir, Y. Zakari, A. I. Kabuga, L. D. Rogo
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摘要

目的:人类免疫缺陷病毒(HIV)是一种慢病毒,可引起HIV感染并随着时间的推移而引起获得性免疫缺陷综合征。目的是评估艾滋病毒阳性和阴性个体的血浆钙网蛋白(CALR)水平。方法:共招募164名参与者,根据病毒载量估计分为四组,并招募个体作为对照组。根据制造商(COBAS Taqman HIV-1定量测试,v2.0,罗氏诊断有限公司,德国),估计1.1 ml血浆中的病毒载量。使用ELISA (ELISA- biotuva Life Sciences, UK)分析血浆CALR水平。结果:低病毒载量个体与未抑制病毒载量个体、抑制病毒载量个体和对照组的CALR水平有显著差异(p = 0.00)。与病毒载量被抑制的个体相比,未抑制病毒载量的个体血浆CALR显著(p = 0.017)升高。未抑制病毒载量的个体与对照组血浆CALR水平无差异。结论:我们的研究显示了长期抗逆转录病毒治疗的hiv感染者血浆CALR的调节。我们相信,从现有的文献来看,这种向上调节部分是由于抗逆转录病毒药物引起的氧化应激和内质网应激。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Plasma Levels of Secretory Calreticulin among HIV Infected Patients in Bauchi State
Objectives: Human immunodeficiency virus (HIV) is a lentivirus that causes HIV infection and over time acquired immunodeficiency syndrome. The objective was to evaluate plasma levels of Calreticulin (CALR) in HIV positive and negative individuals. Methods: A total of 164 participants were recruited and divided into four groups according to their viral load after estimation and individuals recruited as controls. Viral load was estimated in 1.1 ml of plasma according to manufacturers (COBAS Taqman HIV-1 Quantitative Test, v2.0, Roche Diagnostic GmbH, Germany). Plasma levels of CALR were analysed using ELISA (ELISA-Biotuva Life Sciences, UK). Results: Result revealed a significant difference (p = 0.00) between the CALR levels of individuals with low viral load and individuals with unsuppressed viral load, suppressed viral load, and controls. A significantly (p = 0.017) higher plasma CALR in individuals with unsuppressed viral load compared to those with suppressed viral load was found. No differences between plasma CALR levels of individuals with unsuppressed viral load and that of controls. Conclusion: Our study showed up regulation of plasma CALR in HIV-infected patients on long term antiretroviral therapy. We believe and from existing literature this up regulation is due partly if not solely to the oxidative stress and endoplasmic reticulum stress caused by the antiretroviral agents.
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