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Shortened telomeres in the expanded CD28-CD8+ cell subset in HIV disease implicate replicative senescence in HIV pathogenesis
AIDS · 1996 · Vol. 10(8) · pp. F17–22
Rita B. Effros✉(University of California, Los Angeles)Richard AllsoppChoy‐Pik ChiuMary Ann HausnerKarim F. HirjiLili WangCalvin B. HarleyBryant VilleponteauMichael D. WestJanis V. Giorgi
Abstract
The shortened telomeres in the CD28-CD8+ cells in HIV-infected subjects and the poor proliferative potential of these cells identifies CD8+ cell replicative senescence as a newly described feature of HIV disease. Our results provide a mechanism for the loss of CD8+ cell control of viral replication that accompanies advanced HIV disease. Replicative senescence may contribute to exhaustion of the T-cell response as a result of chronic HIV disease. Whether this phenomenon occurs in other chronic viral infections is unknown.
Cytomegalovirus and herpesvirus researchTelomeres, Telomerase, and SenescenceHIV Research and TreatmentTelomereSenescencePathogenesisBiologyVirologyHuman immunodeficiency virus (HIV)DiseaseCD8ImmunologyGenetics
MeSH terms
Cell DivisionDNAHumansMolecular WeightHIV InfectionsT-Lymphocyte SubsetsTelomereCellular SenescenceCD28 AntigensCD8-Positive T-Lymphocytes
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