ArticleiScience2024
Inhibition of HIV-1 replication by nanobodies targeting tetraspanin CD9.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Engineering Protein-Based HIV Entry Inhibitors: Advances, Challenges, and Translational Strategies.Biomolecules · 2026Review
- Article
- Review
- Lipids, Tetraspanins, and Exosomes: Cell Factors inViruses · 2025Review
- Persistent Type I Interferon Signaling Impairs Innate Lymphoid Cells During HIV-1 Infection Under Suppressive ART.Viruses · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-1 alters the dynamics and distribution of tetraspanins, a group of proteins integral to membrane organization, to facilitate both entry and egress. Notably, the tetraspanin CD9 is dysregulated during HIV-1 infection, correlating with multifaceted effects on viral replication. Here, we generated llama-derived nanobodies against CD9 to restrict HIV-1 replication. We immunized llamas with recombinant large extracellular loop of CD9 and identified eight clonally distinct nanobodies targeting CD9, each exhibiting a range of affinities and differential binding to cell surface-expressed CD9. Notably, nanobodies T2C001 and T2C002 demonstrated low nanomolar affinities and exhibited differential sensitivities against endogenous and overexpressed CD9 on the cell surface. Although CD9-directed nanobodies did not impede the early stages of HIV-1 life cycle, they effectively inhibited virus-induced syncytia formation and virus replication in T cells and monocyte-derived macrophages. This discovery opens new avenues for host-targeted therapeutic strategies, potentially augmenting existing antiretroviral treatments for HIV-1.
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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.