Human immunodeficiency virus-1 infection requires pertussis toxin sensitive G-protein-coupled signalling and mediates cAMP downregulation
| Autor: | Keith E. Nye, Amer Qureshi, Brendan J. Murphy, Peter A. M. Eagles, Richard Qihao Zheng, Christine Guntermann |
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| Rok vydání: | 1999 |
| Předmět: |
Receptors
CXCR4 Time Factors G protein Cell Survival Lactams Macrocyclic Biophysics HIV Core Protein p24 Down-Regulation Fluorescent Antibody Technique Biology GTP-Binding Protein alpha Subunits Gi-Go Pertussis toxin Virus Replication Biochemistry CXCR4 Virus Downregulation and upregulation Viral entry GTP-Binding Proteins Benzoquinones Cyclic AMP Humans Lymphocytes Virulence Factors Bordetella Receptor Molecular Biology Quinones Cell Biology Protein-Tyrosine Kinases Flow Cytometry Molecular biology Pertussis Toxin Rifabutin CD4 Antigens HIV-1 Intracellular Cell Division Signal Transduction |
| Zdroj: | Biochemical and biophysical research communications. 256(2) |
| ISSN: | 0006-291X |
| Popis: | The human immunodeficiency virus-1 (HIV-1) utilises CD4 and certain β-chemokine receptors, mainly CCR-5 and CXCR4, for attachment and virus entry into T-lymphocytes and monocytes/macrophages. CD4 and β-chemokine receptors participate in intracellular signalling via protein tyrosine kinases and G-protein-coupled signalling. The factors which influence HIV-1 replication and the intracellular signalling mechanisms elicited by the virus are not well understood. In this study, it was demonstrated that exposure of peripheral blood lymphocytes (PBLs) to a T-cell tropic strain of HIV-1 evokes signal(s) which results in downregulation of intracellular cAMP. In addition, pre-incubation of PBLs with the G i -protein inhibitor Pertussis toxin mediated a significant inhibition of HIV-1 replication. These data strongly suggest that HIV-1 employs CD4 receptors and G i -coupled proteins for entry into target cells and that productive HIV-1 infection is dependent on an active signalling event. |
| Databáze: | OpenAIRE |
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