Knowledge about HIV infection in older persons is becoming increasingly important. CD4+ T cells are essential for protective immunity, but little is known about the effect of age on the CD4+ T-cell impairment in HIV infection.
Treatment-naive patients aged older than 50 or younger than 40 years were studied for absolute and relative frequencies of CD31+ naive and CD31− naive CD4+ T cells, central memory, effector memory, and terminally differentiated CD4+ T cells, and compared with age-matched controls. In addition, cellular proliferation and cytokine secretion properties were determined. CD4+ T-cell reconstitution was analyzed in older and younger patients with <350 or ≥350 CD4+ T cells per microliter at initiation of combination antiretroviral tharapy (cART).
CD4+ T cells of older but not younger HIV-infected patients showed age-inappropriate low levels of CD31− naive cells, increased levels of effector memory cells, and enhanced interferonγ and interleukin-17 secretion. Impaired CD4+ T-cell composition persisted in patients who initiated cART at <350 CD4+ T cells per microliter. In patients with CD4+ T cells ≥350 per microliter, alterations were less pronounced and were reversible with cART. Compared with age-matched controls, total CD4+ T-cell counts did not differ between treated younger and older HIV-infected patients.
These data demonstrate that aging enhances the CD4+ T-cell impairment in HIV-infected persons mainly by a loss of CD31− naive cells, accumulation of effector memory cells, and increased pro-inflammatory effector functions. Age-related changes in CD4+ T-cell composition can be prevented by an early initiation of cART.
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*Department of Gastroenterology, Infectious Diseases, and Rheumatology, Medical Clinic I, Campus Benjamin Franklin, Charité—University Medicine Berlin, Berlin, Germany; and
†Ärzteforum Seestraβe, Berlin, Germany (Heiko Karcher is now with Ärzteforum Praxis City Ost, Berlin, Germany; Desiree Kunkel is now with Berlin–Brandenburg Center for Regenerative Therapies, Campus Virchow Klinikum, Charité—University Medicine Berlin, Berlin, Germany).
Correspondence to: Kristina Allers, PhD, Department of Gastroenterology, Infectious Diseases, and Rheumatology, Medical Clinic I, Campus Benjamin Franklin, Charité, Hindenburgdamm 30, 12203 Berlin, Germany (e-mail: email@example.com).
Supported by research funding from the Deutsche Forschungsgemeinschaft (German Research Foundation, grant SCHN 616/6-1).
The authors have no conflicts of interest to disclose.
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Received December 18, 2013
Accepted December 18, 2013