ArticleProceedings of the National Academy of Sciences of the United States of America2002
HIV-1 matrix protein p17 increases the production of proinflammatory cytokines and counteracts IL-4 activity by binding to a cellular receptor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 63 citations in OpenAlex.
- Role of HIV-1 matrix protein p17 variants in lymphoma pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2015Trial
- Beyond Viral Assembly: The Emerging Role of HIV-1 p17 in Vascular Inflammation and Endothelial Dysfunction.International journal of molecular sciences · 2025Review
- Molecular Mechanisms Involved in the B Cell Growth and Clonogenic Activity of HIV-1 Matrix Protein p17 Variants.Viruses · 2024Article
- HIV-1 Structural Proteins or Cell-Signaling Factors? That Is the Question!Current issues in molecular biology · 2024Review
- The HIV-1 Gag Protein Displays Extensive Functional and Structural Roles in Virus Replication and Infectivity.International journal of molecular sciences · 2022Review
- Evolution toward beta common chain receptor usage links the matrix proteins of HIV-1 and its ancestors to human erythropoietin.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- HIV Antibody Profiles in HIV Controllers and Persons With Treatment-Induced Viral Suppression.Frontiers in immunology · 2021Article
- Role of Autophagy in Von Willebrand Factor Secretion by Endothelial Cells and in the In Vivo Thrombin-Antithrombin Complex Formation Promoted by the HIV-1 Matrix Protein p17.International journal of molecular sciences · 2020Article
- Heparin and heparan sulfate proteoglycans promote HIV-1 p17 matrix protein oligomerization: computational, biochemical and biological implications.Scientific reports · 2019Article
- p17 from HIV induces brain endothelial cell angiogenesis through EGFR-1-mediated cell signalling activation.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- TLR10 Senses HIV-1 Proteins and Significantly Enhances HIV-1 Infection.Frontiers in immunology · 2019Article
- Role of Autophagy in HIV-1 Matrix Protein p17-Driven Lymphangiogenesis.Journal of virology · 2017Article
- HIV-1 matrix protein p17 and its variants promote human triple negative breast cancer cell aggressiveness.Infectious agents and cancer · 2017Article
- Cellular aspartyl proteases promote the unconventional secretion of biologically active HIV-1 matrix protein p17.Scientific reports · 2016Article
- Effect of Glu12-His89 Interaction on Dynamic Structures in HIV-1 p17 Matrix Protein Elucidated by NMR.PloS one · 2016Article
- HIV-associated lymphoma in the era of combination antiretroviral therapy: shifting the immunological landscape.Pathogens and disease · 2015Review
- HIV-1 Structural Proteins Serve as PAMPs for TLR2 Heterodimers Significantly Increasing Infection and Innate Immune Activation.Frontiers in immunology · 2015Article
- Association of VH4-59 Antibody Variable Gene Usage with Recognition of an Immunodominant Epitope on the HIV-1 Gag Protein.PloS one · 2015Article
- Simian immunodeficiency virus and human immunodeficiency virus type 1 matrix proteins specify different capabilities to modulate B cell growth.Journal of virology · 2014Article
- Ruxolitinib and tofacitinib are potent and selective inhibitors of HIV-1 replication and virus reactivation in vitro.Antimicrobial agents and chemotherapy · 2014Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purified recombinant HIV-1 p17 matrix protein significantly increased HIV-1 replication in preactivated peripheral blood mononuclear cell cultures obtained from healthy donors. Because HIV-1 infection and replication is related to cell activation and differentiation status, in the present study, we investigated the role played by p17 during the process of T cell stimulation. Using freshly isolated peripheral blood mononuclear cells, we demonstrate that p17 was able to enhance levels of tumor necrosis factor alpha and IFN-gamma released from cells stimulated by IL-2. IL-4 was found to down-regulate IFN-gamma and tumor necrosis factor alpha, and p17 restored the ability of cells to produce both cytokines. The property of p17 to increase production of proinflammatory cytokines could be a mechanism exploited by the virus to create a more suitable environment for HIV-1 infection and replication. Our data show that p17 exerts its biological activity after binding to a specific cellular receptor expressed on activated T lymphocytes. The functional p17 epitope involved in receptor binding was found to be located at the NH(2)-terminal region of viral protein. Immunization of BALB/c mice with a 14-aa synthetic peptide representative of the HIV-1 p17 functional region (SGGELDRWEKIRLR) resulted in the development of p17 neutralizing antibodies capable of blocking the interaction between p17 and its cellular receptor. Our results define a role for p17 in HIV-1 pathogenesis and contribute to our understanding of the molecular mechanism of HIV-1 infection and the development of additional antiviral therapeutic strategies.
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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.