ArticleProceedings of the National Academy of Sciences of the United States of America2020
PSGL-1 restricts HIV-1 infectivity by blocking virus particle attachment to target cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 65 citations in OpenAlex.
- Versatile HIV Rev-dependent reporter cell system for stringent and sensitive quantification of viral reservoirs, neutralizing antibodies, and restriction factors.Retrovirology · 2026Article
- P-Selectin Glycoprotein Ligand (PSGL)-1 Expression on CD4Pathogens (Basel, Switzerland) · 2025Observational
- Versatile HIV Rev-dependent reporter cell system for stringent and sensitive quantification of viral reservoirs, neutralizing antibodies, and restriction factors.bioRxiv : the preprint server for biology · 2025Article
- Assembly of CCR5 with gp120 inhibits the HIV infectivity specifically in T cells.Scientific reports · 2025Article
- Mechanisms of Immune Evasion in HIV-1: The Role of Virus-Host Protein Interactions.Current issues in molecular biology · 2025Review
- PIPScience advances · 2025Article
- PSGL-1 excludes HIV Env from virion surface through spatial hindrance involving structural folding of the decameric repeats (DR).bioRxiv : the preprint server for biology · 2024Article
- Review
- HIV-1 Vpu induces neurotoxicity by promoting Caspase 3-dependent cleavage of TDP-43.EMBO reports · 2024Article
- Review
- Characterization of a CXCR4 antagonist TIQ-15 with dual tropic HIV entry inhibition properties.PLoS pathogens · 2024Article
- Antiviral factors and their counteraction by HIV-1: many uncovered and more to be discovered.Journal of molecular cell biology · 2024Review
- Article
- The role of P-selectin/PSGL-1 in regulating NETs as a novel mechanism in cerebral ischemic injury.Frontiers in neurology · 2024Review
- Interactions between HIV proteins and host restriction factors: implications for potential therapeutic intervention in HIV infection.Frontiers in immunology · 2024Review
- Identification of CD38, CD97, and CD278 on the HIV surface using a novel flow virometry screening assay.Scientific reports · 2023Article
- PSGL-1, a Strategic Biomarker for Pathological Conditions in HIV Infection: A Hypothesis Review.Viruses · 2023Review
- E3 Ubiquitin Ligases in Gammaherpesviruses and HIV: A Review of Virus Adaptation and Exploitation.Viruses · 2023Review
- HIV Infection: Shaping the Complex, Dynamic, and Interconnected Network of the Cytoskeleton.International journal of molecular sciences · 2023Review
- Article
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
P-selectin glycoprotein ligand-1 (PSGL-1) is a dimeric, mucin-like, 120-kDa glycoprotein that binds to P-, E-, and L-selectins. PSGL-1 is expressed primarily on the surface of lymphoid and myeloid cells and is up-regulated during inflammation to mediate leukocyte tethering and rolling on the surface of endothelium for migration into inflamed tissues. Although it has been reported that PSGL-1 expression inhibits HIV-1 replication, the mechanism of PSGL-1-mediated anti-HIV activity remains to be elucidated. Here we report that PSGL-1 in virions blocks the infectivity of HIV-1 particles by preventing the binding of particles to target cells. This inhibitory activity is independent of the viral glycoprotein present on the virus particle; the binding of particles bearing the HIV-1 envelope glycoprotein or vesicular stomatitis virus G glycoprotein or even lacking a viral glycoprotein is impaired by PSGL-1. Mapping studies show that the extracellular N-terminal domain of PSGL-1 is necessary for its anti-HIV-1 activity, and that the PSGL-1 cytoplasmic tail contributes to inhibition. In addition, we demonstrate that the PSGL-1-related monomeric E-selectin-binding glycoprotein CD43 also effectively blocks HIV-1 infectivity. HIV-1 infection, or expression of either Vpu or Nef, down-regulates PSGL-1 from the cell surface; expression of Vpu appears to be primarily responsible for enabling the virus to partially escape PSGL-1-mediated restriction. Finally, we show that PSGL-1 inhibits the infectivity of other viruses, such as murine leukemia virus and influenza A virus. These findings demonstrate that PSGL-1 is a broad-spectrum antiviral host factor with a unique mechanism of action.
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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.