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APOL1 Renal Risk Variants: Fertile Soil for HIV-Associated Nephropathy

  1. Author:
    Kopp, Jeffrey B.
    Heymann, Jurgen
    Winkler, Cheryl

  2. Author Address

    NIDDK, Kidney Dis Sect, NIH, Bethesda, MD USA.NCI, Basic Res Lab, NIH, Leidos Biomed Res,Frederick Natl Lab Canc Res, Frederick, MD 21701 USA.
    1. Year: 2017
    2. Date: Nov
  2. Journal: Seminars in nephrology
  3. W B SAUNDERS CO-ELSEVIER INC,
    1. 37
    2. 6
    3. Pages: 514-519
  5. Type of Article: Review
  6. ISSN: 0270-9295
  1. Abstract:

    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 1 b 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. Published by Elsevier Inc.

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External Sources

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  2. DOI: 10.1016/j.semnephrol.2017.07.004
  3. PMID: 29110758
  4. View record in Web of Science®
  5. WOS: 000413617500004

Library Notes

  1. Fiscal Year: FY2017-2018
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