ArticleRetrovirology2016
Impact of APOL1 polymorphism and IL-1β priming in the entry and persistence of HIV-1 in human podocytes.
Article in Retrovirology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Apolipoprotein L1 gene variants and kidney disease in patients with HIV: a systematic review and meta-analysis.Journal of nephrology · 2023Pooled it
- APOL1 Genotype and Patient Outcomes in US and South African Transplant Recipients With HIV who Received Kidneys From Donors With HIV.Transplantation · 2026Article
- Collapsing Glomerulopathy in Brazil: A Nationwide Descriptive Study.Nephrology (Carlton, Vic.) · 2025Article
- Carrying APOL1 G1 allele is associated with cardiovascular complications during COVID-19 in an admixed population.Human genomics · 2025Article
- Article
- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.Biomedicines · 2024Review
- IFI16 Is Indispensable for Promoting HIF-1α-Mediated APOL1 Expression in Human Podocytes under Hypoxic Conditions.International journal of molecular sciences · 2024Article
- Characterization of immortalized human podocytes infected with lentivirus as anAmerican journal of clinical and experimental immunology · 2024Article
- APOL1 risk variants and the development of HIV-associated nephropathy.The FEBS journal · 2021Review
- Collapsing Focal Segmental Glomerulosclerosis in Viral Infections.Frontiers in immunology · 2021Review
- HIV Viremia Is Associated WithFrontiers in medicine · 2021Article
- APOL1 polymorphism modulates sphingolipid profile of human podocytes.Glycoconjugate journal · 2020Article
- Apolipoprotein L1-Specific Antibodies Detect Endogenous APOL1 inside the Endoplasmic Reticulum and on the Plasma Membrane of Podocytes.Journal of the American Society of Nephrology : JASN · 2020Article
- APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin.Cell reports · 2020Article
- Article
- Disrupted apolipoprotein L1-miR193a axis dedifferentiates podocytes through autophagy blockade in an APOL1 risk milieu.American journal of physiology. Cell physiology · 2019Article
- APOL1 and kidney cell function.American journal of physiology. Renal physiology · 2019Review
- First report of collapsing variant of focal segmental glomerulosclerosis triggered by arbovirus: dengue and Zika virus infection.Clinical kidney journal · 2019Article
- Common Mechanisms of Viral Injury to the Kidney.Advances in chronic kidney disease · 2019Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
backgroundPatients of African ancestry with untreated HIV-1 infection and carrying the G1 or G2 kidney disease risk variants (Vs) at the APOL1 gene have a tenfold higher risk of developing HIV-associated nephropathy (HIVAN) compared to those with the non-risk wild type (WT) G0 variant. However, the mechanistic contribution of the APOL1 allelic state to kidney injury in HIV-1 infection remains to be elucidated.
resultsNon-risk WT APOL1 is associated with lower intracellular levels of HIV-1 in conditionally immortalized human podocytes, while the over expression of G1 or G2 risk Vs significantly increases viral accumulation. The priming of podocytes with exogenous IL-1β facilitates HIV-1 entry, via the up-regulation of DC-SIGN. The over expression of APOL1 G1 and G2 risk Vs in combination with an increase in IL-1β levels causes a greater increase in viral concentration than either condition alone. In turn, HIV-1 and exogenous IL-1β together induce a de novo secretion of endogenous IL-1β and an increase of APOL1 gene expression.
conclusionsOur findings indicate that the presence of risk Vs of APOL1 is permissive of HIV-1 persistence in human podocytes in synergy with IL-1β, a cytokine that characterizes the inflammatory milieu of acute and chronic phases of HIV-1 infection. The elucidation of these molecular mechanisms explains, at least in part, the higher frequency of HIVAN in populations carrying the risk polymorphic genetic variant of APOL1 gene.
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