These authors contributed equally to this work.
Expression of p16INK4a as a biomarker of T-cell aging in HIV-infected patients prior to and during antiretroviral therapy
Article first published online: 19 JUL 2012
© 2012 The Authors. Aging Cell © 2012 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland
Volume 11, Issue 5, pages 916–918, October 2012
How to Cite
Nelson, J. A. E., Krishnamurthy, J., Menezes, P., Liu, Y., Hudgens, M. G., Sharpless, N. E. and Eron, J. J. (2012), Expression of p16INK4a as a biomarker of T-cell aging in HIV-infected patients prior to and during antiretroviral therapy. Aging Cell, 11: 916–918. doi: 10.1111/j.1474-9726.2012.00856.x
- Issue published online: 16 SEP 2012
- Article first published online: 19 JUL 2012
- Accepted manuscript online: 27 JUN 2012 10:17AM EST
- Accepted for publication 15 June 2012
- T cell;
The p16INK4a tumor suppressor gene is a mediator of cellular senescence and has been suggested to be a biomarker of ‘molecular’ age in several tissues including T cells. To determine the association of both active and suppressed HIV infection with T-cell aging, T-cell p16INK4a expression was compared between 60 HIV+ suppressed subjects, 23 HIV+ untreated subjects, and 18 contemporaneously collected HIV-negative controls, as well as 148 HIV-negative historical samples. Expression did not correlate with chronologic age in untreated HIV+ patients, consistent with an effect of active HIV replication on p16INK4a expression. In patients on cART with suppressed viral loads, however, p16INK4a levels were similar to uninfected controls and correlated with chronologic age, with a trend toward an inverse correlation with CD4 count. These data show that p16INK4a is a reliable biomarker of T-cell aging in HIV+ patients with suppressed viral loads and suggest that poor CD4 cell recovery on cART may be associated with increased T-cell expression of p16INK4a, a marker of cellular senescence.