ArticleCell death & disease2020
SMAC mimetics induce autophagy-dependent apoptosis of HIV-1-infected macrophages.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Methaneseleninic acid, a circadian-modulating agent, reactivates latent HIV-1 infection without cellular activation or proliferation.Journal of virology · 2026Article
- Review
- Sex-Specific Factors Influencing HIV Infection.Immunological reviews · 2026Review
- Host-directed approaches in the pursuit of a cure for HIV.Antiviral research · 2025Review
- The inducible role of autophagy in cell death: emerging evidence and future perspectives.Cell communication and signaling : CCS · 2025Review
- Effect and mechanism of miRNA-144-5p-regulated autophagy in older adults with Sarcopenia.Immunity & ageing : I & A · 2025Article
- ABT-263, a BCL-2 inhibitor, selectively eliminates latently HIV-1-infected cells without viral reactivation.PloS one · 2025Article
- SMAC mimetics sensitize HIV-infected cells to oncolytic virus-mediated death.Frontiers in immunology · 2025Article
- Bivalent SMAC mimetic APG-1387 reduces HIV reservoirs and limits viral rebound in humanized mice.iScience · 2024Article
- Review
- Noncanonical-NF-κB activation and DDX3 inhibition reduces the HIV-1 reservoir by elimination of latently infected cellsMicrobiology spectrum · 2024Article
- Molecular basis for nuclear accumulation and targeting of the inhibitor of apoptosis BIRC2.Nature structural & molecular biology · 2023Article
- IRAK1 inhibition blocks the HIV-1 RNA mediated pro-inflammatory cytokine response from microglia.The Journal of general virology · 2023Article
- BCL-2-family protein tBID can act as a BAX-like effector of apoptosis.The EMBO journal · 2022Article
- Current strategies to induce selective killing of HIV-1-infected cells.Journal of leukocyte biology · 2022Review
- The role of latency reversal in HIV cure strategies.Journal of medical primatology · 2022Review
- Article
- So Pathogenic or So What?-A Brief Overview of SIV Pathogenesis with an Emphasis on Cure Research.Viruses · 2022Review
- CounterAKTing HIV: Toward a "Block and Clear" Strategy?Frontiers in cellular and infection microbiology · 2022Review
- Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Human immunodeficiency type 1 (HIV)-infected macrophages (HIV-Mφ) are a reservoir for latent HIV infection and a barrier to HIV eradication. In contrast to CD4+ T cells, HIV-Mφ are resistant to the cytopathic effects of acute HIV infection and have increased expression of cell survival factors, including X-linked inhibitor of apoptosis (XIAP), baculoviral IAP repeat containing (BIRC) 2/cIAP1, beclin-1, BCL2, BCL-xl, triggering receptor expressed on myeloid cells 1, mitofusin (MFN) 1, and MFN2. DIABLO/SMAC mimetics are therapeutic agents that affect cancer cell survival and induce cell death. We found that DIABLO/SMAC mimetics (LCL-161, AT-406 (also known as SM-406 or Debio 1143), and birinapant) selectively kill HIV-Mφ without increasing bystander cell death. DIABLO/SMAC mimetic treatment of HIV-Mφ-induced XIAP and BIRC2 degradation, leading to the induction of autophagy and the formation of a death-inducing signaling complex on phagophore membranes that includes both pro-apoptotic or necroptotic (FADD, receptor-interacting protein kinase (RIPK) 1, RIPK3, caspase 8, and MLKL) and autophagy (ATG5, ATG7, and SQSTM1) proteins. Genetic or pharmacologic inhibition of early stages of autophagy, but not late stages of autophagy, ablated this interaction and inhibited apoptosis. Furthermore, DIABLO/SMAC mimetic-mediated apoptosis of HIV-Mφ is dependent upon tumor necrosis factor signaling. Our findings thus demonstrate that DIABLO/SMAC mimetics selectively induce autophagy-dependent apoptosis in HIV-Mφ.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.