ArticleThe Journal of experimental medicine1999
The B-oligomer of pertussis toxin deactivates CC chemokine receptor 5 and blocks entry of M-tropic HIV-1 strains.
Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 96 citations in OpenAlex.
- Advancing EAE Modeling: Establishment of a Non-Pertussis Immunization Protocol for Multiple Sclerosis.Bio-protocol · 2026Article
- Co-receptor signaling in the pathogenesis of neuroHIV.Retrovirology · 2021Review
- Pertussis Toxin Inhibits Encephalitogenic T-Cell Infiltration and Promotes a B-Cell-Driven Disease during Th17-EAE.International journal of molecular sciences · 2021Article
- Human Beta-Defensin 2 and 3 Inhibit HIV-1 Replication in Macrophages.Frontiers in cellular and infection microbiology · 2021Article
- A biophysical perspective on receptor-mediated virus entry with a focus on HIV.Biochimica et biophysica acta. Biomembranes · 2020Review
- Lipid rafts and pathogens: the art of deception and exploitation.Journal of lipid research · 2020Review
- Immunomodulation as a Novel Strategy for Prevention and Treatment ofFrontiers in immunology · 2019Review
- Novel Therapeutic Approach for Inhibition of HIV-1 Using Cell-Penetrating Peptide and Bacterial Toxins.Journal of AIDS & clinical research · 2017Article
- Chemoattractant-mediated leukocyte trafficking enables HIV dissemination from the genital mucosa.JCI insight · 2017Article
- HIV-1 triggers WAVE2 phosphorylation in primary CD4 T cells and macrophages, mediating Arp2/3-dependent nuclear migration.The Journal of biological chemistry · 2014Article
- Use of G-protein-coupled and -uncoupled CCR5 receptors by CCR5 inhibitor-resistant and -sensitive human immunodeficiency virus type 1 variants.Journal of virology · 2013Article
- CXCR4-tropic, but not CCR5-tropic, human immunodeficiency virus infection is inhibited by the lipid raft-associated factors, acyclic retinoid analogs, and cholera toxin B subunit.AIDS research and human retroviruses · 2013Article
- Pertussis toxin exacerbates and prolongs airway inflammatory responses during Bordetella pertussis infection.Infection and immunity · 2012Article
- Early events of HIV-1 infection: can signaling be the next therapeutic target?Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011Review
- Asymmetric HIV-1 co-receptor use and replication in CD4(+) T lymphocytes.Journal of translational medicine · 2011Review
- Virus-induced Ca2+ influx extends survival of west nile virus-infected cells.Journal of virology · 2010Article
- Review
- The macrophage in HIV-1 infection: from activation to deactivation?Retrovirology · 2010Review
- Pertussis toxin and adenylate cyclase toxin: key virulence factors of Bordetella pertussis and cell biology tools.Future microbiology · 2010Review
- Differential contribution of chemotaxis and substrate restriction to segregation of immature and mature thymocytes.Immunity · 2009Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection of target cells by HIV-1 requires initial binding interactions between the viral envelope glycoprotein gp120, the cell surface protein CD4, and one of the members of the seven-transmembrane G protein-coupled chemokine receptor family. Most primary isolates (R5 strains) use chemokine receptor CCR5, but some primary syncytium-inducing, as well as T cell line-adapted, strains (X4 strains) use the CXCR4 receptor. Signaling from both CCR5 and CXCR4 is mediated by pertussis toxin (PTX)-sensitive G(i) proteins and is not required for HIV-1 entry. Here, we show that the PTX holotoxin as well as its binding subunit, B-oligomer, which lacks G(i)-inhibitory activity, blocked entry of R5 but not X4 strains into primary T lymphocytes. Interestingly, B-oligomer inhibited virus production by peripheral blood mononuclear cell cultures infected with either R5 or X4 strains, indicating that it can affect HIV-1 replication at both entry and post-entry levels. T cells treated with B-oligomer did not initiate signal transduction in response to macrophage inflammatory protein (MIP)-1beta or RANTES (regulated upon activation, normal T cell expressed and secreted); however, cell surface expression of CCR5 and binding of MIP-1beta or HIV-1 to such cells were not impaired. The inhibitory effect of B-oligomer on signaling from CCR5 and on entry of R5 HIV-1 strains was reversed by protein kinase C (PKC) inhibitors, indicating that B-oligomer activity is mediated by signaling events that involve PKC. B-oligomer also blocked cocapping of CCR5 and CD4 induced by R5 HIV-1 in primary T cells, but did not affect cocapping of CXCR4 and CD4 after inoculation of the cultures with X4 HIV-1. These results suggest that the B-oligomer of PTX cross-deactivates CCR5 to impair its function as a coreceptor for HIV-1.
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