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首页> 外文期刊>Seminars in Nephrology >APOL1 Renal Risk Variants: Fertile Soil for HIV-Associated Nephropathy
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APOL1 Renal Risk Variants: Fertile Soil for HIV-Associated Nephropathy

机译：Apol1肾风险变体：艾滋病毒相关肾病的肥沃土壤

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Summary: Apolipoprotein L1 ( APOL1 ) genetic variants are potent risk factors for glomerular disease, but one or more additional factors are required for expression of glomerular disease. Uncontrolled or poorly controlled human immunodeficiency virus (HIV) infection is the most potent susceptibility factor for APOL1 nephropathy that has been identified to date. APOL1 variants are associated with HIV-associated nephropathy (HIVAN), a podocyte disease, but not with HIV-immune complex disease, primarily a disease of the mesangium. The mechanism by which HIV brings out the latent glomerular disease risk remains to be defined. There are at least two classes of candidate mechanisms to explain the potent interaction between HIV-1 and APOL1 . First, APOL1 variant proteins and HIV accessory proteins implicated in HIVAN may target the same or related intracellular pathways in podocytes. Recent data suggest roles for interleukin 1b and transcription factor EB. Second, features of uncontrolled HIV infection, including increased circulating factors such as interferon, may drive APOL1 gene transcription or act upon podocytes in other ways. Deeper probing of APOL1 –HIV interactions may yield insights that will aid in understanding HIVAN, APOL1 nephropathy, and podocyte biology.
机译：发明内容：载脂蛋白L1（APOL1）遗传变异是肾小球疾病的有效危险因素，但表达肾小球疾病需要一种或多种因素。人类免疫缺陷病毒（HIV）感染的不受控制或贫瘠的贫瘠或贫困性是最有效的易感性因素，其已被确定为迄今为止。 Apol1变体与艾滋病毒相关的肾病（HiVAN），雌细胞疾病，但不适用于艾滋病毒免疫复合疾病，主要是Mesangium的疾病。 HIV产生潜在肾小球疾病风险的机制仍有待确定。至少有两种候选机制来解释HIV-1和APOL1之间的有效相互作用。首先，Apol1变体蛋白和艾滋病毒辅助蛋白与HiVAN有关的蛋白质可以靶向多粒细胞中的相同或相关的细胞内途径。最近的数据表明白细胞介素1B和转录因子EB的作用。其次，不受控制的艾滋病毒感染的特征，包括增加循环因子，如干扰素，可以以其他方式驱动Apol1基因转录或作用于多粒细胞。深度探讨APOL1-HIV相互作用可能会产生有助于了解HIVAN，APOL1肾病和多粒细节生物学的见解。

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