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Human immunodeficiency virus-associated changes in signal transduction.
1Department of Medicine, University of California, Irvine 92717.
Journal of Clinical Immunology
|November 1, 1987
Summary
Human immunodeficiency virus (HIV) disrupts T-cell signaling by altering membrane potential and calcium levels. This dysfunction in T-cell activation pathways may explain T-cell impairment in HIV infection.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- T-cell activation involves critical signaling events like calcium ([Ca2+]i) flux and membrane potential changes.
- These early events are essential for downstream T-cell responses, including proliferation and lymphokine production.
- Human immunodeficiency virus (HIV) is known to cause T-cell dysfunction.
Purpose of the Study:
- To investigate the impact of HIV infection on T-cell membrane potential and intracellular calcium levels.
- To understand how HIV affects the early signal transduction pathways of T-cell activation.
Main Methods:
- Utilized T cell lines, including HIV-infected (H9/HTLV IIIb) and uninfected (H9) counterparts.
- Measured membrane potential and intracellular calcium ([Ca2+]i) levels.
- Stimulated T cells with phytohemagglutinin (PHA) and anti-T3 monoclonal antibody to assess activation responses.
Main Results:
- HIV-infected T cells (H9/HTLV IIIb) exhibited decreased (depolarized) membrane potentials compared to uninfected cells.
- Basal [Ca2+]i levels were elevated in HIV-infected T cells.
- HIV-infected T cells showed a blunted [Ca2+]i response upon stimulation with PHA or anti-T3, unlike uninfected cells.
- These findings indicate impaired signal transduction in HIV-infected T cells.
Conclusions:
- Chronic HIV infection leads to significant abnormalities in T-cell plasma membrane potential and intracellular calcium handling.
- These disruptions in T-cell activation signaling pathways are likely contributors to the immunodeficiency observed in HIV-infected individuals.