Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 107, Issue 2, Pages 207-215Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI11109
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI040384] Funding Source: NIH RePORTER
- NIAID NIH HHS [R01 AI40384, R01 AI040384] Funding Source: Medline
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There is considerable confusion concerning the mechanism of lymphocyte death during HIV infection. During the course of HIV infection, M-tropic viruses (R5) that use CCR5 chemokine coreceptors frequently evolve to T-tropic viruses (X4) that use CXCR4 receptors. In this study we show that activation of the CD4 or CCR5 receptor by R5 HIVenv causes a caspase 8-dependent death of both uninfected and infected CD4 T cells. In contrast, CXCR4 activation by X4 HIVenv induces a caspase-independent death of both uninfected CD4 and CD8 T cells and infected CD4 cells. These results suggest that activation of the chemokine receptor by HIVenv determines the mechanism of death for both infected and uninfected T lymphocytes.
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