Volume 5 Supplement 1
T cell immunosenescence is associated with the presence of Kaposi’s sarcoma in antiretroviral treated human immunodeficiency virus-infected persons
© Unemori et al; licensee BioMed Central Ltd. 2010
Published: 11 October 2010
We reported an atypical cohort of antiretroviral-treated patients who developed or had unremitting Kaposi’s sarcoma (KS) despite having undetectable viral loads and high CD4 cell counts. The KS course of these patients is indolent, resembling elderly or classical HIV- KS. Since HIV infection is associated with accelerated immunologic aging (“immunosenescence”), and since classical HIV- KS of the elderly may be related to age-associated T cell dysfunction, we hypothesized that T cell immunosenescence would be associated with the presence of this atypical KS.
Materials and methods
We identified 19 individuals on antiretroviral therapy (ART) who developed or had unremitting KS after an interval of at least 24 months with viral loads <75 copies RNA/mL and peripheral CD4 cell counts >300 cells/mm3. We also recruited 47 HIV+ KS- controls on ART with viral loads <75 copies RNA/mL and peripheral CD4 cell counts >300 cells/mm3. Global immunosenescence markers CD28 and CD57, as well as naïve cell phenotypic coexpression of CD27+/CD28+/CD45RA+, were examined in peripheral blood via flow cytometry.
Age and Markers of HIV Infection in HIV+ KS+ Cases and HIV+ KS- Controls.
Number of Subjects (N)
Median Age (years)*
Median CD4 cell count (cells/mm3)
Median CD8 cell count (cells/mm3)
Median Viral Load (copies RNA/mL)
HIV+ KS+ Cases
HIV+ KS- Controls
The indolent KS observed among antiretroviral-treated patients is associated with a higher frequency of immunosenescent T cells, characterized by global immunosenescence markers and decreased numbers of naive cells. These markers provide more evidence that KS in these patients may be a consequence of enduring HIV-associated T cell dysfunction and T cell immunosenescence. This association of immunosenescence in otherwise well-treated HIV infection with an AIDS-defining malignancy may provide important insights into the role of immune dysfunction as a cause of premature morbidity commonly observed in the HIV+ cohorts.
This article has been published as part of Infectious Agents and Cancer Volume 5 Supplement 1, 2010: Proceedings of the 12th International Conference on Malignancies in AIDS and Other Acquired Immunodeficiencies (ICMAOI).The full contents of the supplement are available online at http://www.biomedcentral.com/1750-9378/5?issue=S1.
This article is published under license to BioMed Central Ltd.