ArticleNature communications2017
HIV-1 counteracts an innate restriction by amyloid precursor protein resulting in neurodegeneration.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 63 citations in OpenAlex.
- Review
- From infection to dysfunction: viral triggers and antiviral immune factors in Alzheimer's disease pathology.Frontiers in immunology · 2026Review
- HIF-1 Targeting Intervention Renders Protection From Alzheimer's-Like Pathology in a Humanized Mice Model of HIV Infection.Journal of extracellular vesicles · 2025Article
- Human immunodeficiency virus 1 glycoprotein 120 induces endoplasmic reticulum stress in neurons.Cell death & disease · 2025Article
- Transient receptor potential channels in viral infectious diseases: Biological characteristics and regulatory mechanisms.Journal of advanced research · 2025Review
- Negative interplay between HIV-1 Gag and amyloid precursor protein centers around competition for VPS4A and TSG101.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Systemic inflammation as a central player in the initiation and development of Alzheimer's disease.Immunity & ageing : I & A · 2025Review
- Human Brain Organoids: Development and Applications.Journal of microbiology and biotechnology · 2025Review
- Microglial cGAS Deletion Preserves Intercellular Communication and Alleviates Amyloid-β-Induced Pathogenesis of Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Inflammatory responses revealed through HIV infection of microglia-containing cerebral organoids.Journal of neuroinflammation · 2025Article
- α-Synuclein fibrils enhance HIV-1 infection of human T cells, macrophages and microglia.Nature communications · 2025Article
- Effects of West Nile virus on behavioral and cognitive performance, cortical Aβ pathology, viral loads, and immune measures of middle-aged NL-G-F/E3 and NL-G-F/E4 mice.Frontiers in aging neuroscience · 2025Article
- Evaluation of the Anti-Amyloid and Anti-Inflammatory Properties of a Novel Vanadium(IV)-Curcumin Complex in Lipopolysaccharides-Stimulated Primary Rat Neuron-Microglia Mixed Cultures.International journal of molecular sciences · 2024Article
- Histamine stimulates human microglia to alter cellular prion protein expression via the HRH2 histamine receptor.Scientific reports · 2024Article
- Neuropathogenic role of astrocyte-derived extracellular vesicles in HIV-associated neurocognitive disorders.Journal of extracellular vesicles · 2024Article
- Viral Infections, Are They a Trigger and Risk Factor of Alzheimer's Disease?Pathogens (Basel, Switzerland) · 2024Review
- A review of the roles of pathogens in Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Amyloid precursor protein facilitates SARS-CoV-2 virus entry into cells and enhances amyloid-β-associated pathology in APP/PS1 mouse model of Alzheimer's disease.Translational psychiatry · 2023Article
- γ-Secretase fanning the fire of innate immunity.Biochemical Society transactions · 2023Review
- HIV-1 promotes ubiquitination of the amyloidogenic C-terminal fragment of APP to support viral replication.Nature communications · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
While beta-amyloid (Aβ), a classic hallmark of Alzheimer's disease (AD) and dementia, has long been known to be elevated in the human immunodeficiency virus type 1 (HIV-1)-infected brain, why and how Aβ is produced, along with its contribution to HIV-associated neurocognitive disorder (HAND) remains ill-defined. Here, we reveal that the membrane-associated amyloid precursor protein (APP) is highly expressed in macrophages and microglia, and acts as an innate restriction against HIV-1. APP binds the HIV-1 Gag polyprotein, retains it in lipid rafts and blocks HIV-1 virion production and spread. To escape this restriction, Gag promotes secretase-dependent cleavage of APP, resulting in the overproduction of toxic Aβ isoforms. This Gag-mediated Aβ production results in increased degeneration of primary cortical neurons, and can be prevented by γ-secretase inhibitor treatment. Interfering with HIV-1's evasion of APP-mediated restriction also suppresses HIV-1 spread, offering a potential strategy to both treat infection and prevent HAND.
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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.