ArticleAIDS research and human retroviruses2013
Gardiquimod: a Toll-like receptor-7 agonist that inhibits HIV type 1 infection of human macrophages and activated T cells.
Article in AIDS research and human retroviruses, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Microglia-Dependent BDNF Signaling in the Dentate Gyrus Underlies the Antidepressant Effects of Gardiquimod, a Toll-Like Receptor 7 Agonist, in Chronically Stressed Mice.Neurochemical research · 2026Article
- Plasmacytoid dendritic cells are dispensable or detrimental in murine systemic or respiratory viral infections.Nature immunology · 2025Article
- General Approach To Access Aldehyde Oxidase Metabolites of Drug Molecules viaOrganic letters · 2025Article
- Exploring the Role of Pattern Recognition Receptors as Immunostimulatory Molecules.Immunity, inflammation and disease · 2025Review
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- Sensing of an HIV-1-Derived Single-Stranded RNA-Oligonucleotide Induces Arginase 1-Mediated Tolerance.Cells · 2024Article
- Article
- MiR-155 Negatively Regulates Anti-Viral Innate Responses among HIV-Infected Progressors.Viruses · 2023Article
- TIRAP, TRAM, and Toll-Like Receptors: The Untold Story.Mediators of inflammation · 2023Review
- Crosstalk between TLR8 and RIG-I-like receptors enhances antiviral immune responses.Frontiers in medicine · 2023Article
- Inflammatory platelet production stimulated by tyrosyl-tRNA synthetase mimicking viral infection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Relevance of TLR8 in Viral Infections.Pathogens (Basel, Switzerland) · 2022Review
- TLR7 Activation of Macrophages by Imiquimod Inhibits HIV Infection through Modulation of Viral Entry Cellular Factors.Biology · 2021Article
- A Role of Intracellular Toll-Like Receptors (3, 7, and 9) in Response toInternational journal of molecular sciences · 2020Review
- Agonist and antagonist ligands of toll-like receptors 7 and 8: Ingenious tools for therapeutic purposes.European journal of medicinal chemistry · 2020Review
- TLR7 Agonists Display Potent Antiviral Effects against Norovirus Infection via Innate Stimulation.Antimicrobial agents and chemotherapy · 2018Article
- Toll-Like Receptor 7 Agonist GS-9620 Induces HIV Expression and HIV-Specific Immunity in Cells from HIV-Infected Individuals on Suppressive Antiretroviral Therapy.Journal of virology · 2017Article
- TLR7 Agonist GS-9620 Is a Potent Inhibitor of Acute HIV-1 Infection in Human Peripheral Blood Mononuclear Cells.Antimicrobial agents and chemotherapy · 2017Article
- TLR7/8 agonist induces a post-entry SAMHD1-independent block to HIV-1 infection of monocytes.Retrovirology · 2016Article
- In Silico Analysis of Tat Exons to Increase the Efficacy of a Nef-Tat-based HIV-1 Vaccine Candidate.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune response modifiers are being studied as therapeutic agents for viral infections and cancer. These molecules include agonists for the Toll-like receptors (TLR), a family of innate immune receptors. TLR7 and 8, located in cellular endosomes, bind single-stranded RNA characteristic of viral genomes, and trigger intracellular signaling pathways that induce inflammatory cytokines and antiviral innate immune factors. We studied the anti-HIV-1 effects of gardiquimod, a specific TLR7 agonist when used at concentrations below 10 μM, in macrophages and activated peripheral blood mononuclear cells (PBMCs). Gardiquimod, added prior to or within 2 days after infection with X4, R5, or dual-tropic (R5/X4) strains of HIV-1, significantly reduced infection in these cells. Cocultures of activated PBMCs added to gardiquimod-treated and HIV-1-exposed macrophages demonstrated minimal HIV-1 replication for up to 10 days, suggesting that gardiquimod inhibited activated PBMCs viral amplification from HIV-1-exposed macrophages. Gardiquimod treatment of both activated PBMCs and macrophages induced interferon-alpha (IFN-α) transcription within hours of addition, and sustained IFN-α protein secretion for several days. Treatment of cells with a peptide inhibitor to the MyD88 adaptor protein blocked the induction of IFN-α by gardiquimod, and partially reversed the anti-HIV effects in activated PBMCs. Blocking the IFN-α receptor with a neutralizing antibody also reduced the anti-HIV effect of gardiquimod. Gardiquimod inhibited HIV-1 reverse transcriptase, an early step in the life cycle of HIV-1. These findings suggest that gardiquimod, functioning as both an immune system modifier and a reverse transcriptase inhibitor, could be developed as a novel therapeutic agent to block systemic and mucosal transmission of HIV-1.
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