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 Blood, 1 October 2009, Vol. 114, No. 14, pp. 2917-2925.
Prepublished online as a Blood First Edition Paper on April 21, 2009; DOI 10.1182/blood-2009-02-204263.

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IMMUNOBIOLOGY

The level of monocyte turnover predicts disease progression in the macaque model of AIDS

Atsuhiko Hasegawa1, Huining Liu1, Binhua Ling2, Juan T. Borda2, Xavier Alvarez2, Chie Sugimoto1, Heather Vinet-Oliphant2, Woong-Ki Kim3, Kenneth C. Williams3, Ruy M. Ribeiro4, Andrew A. Lackner2, Ronald S. Veazey2, and Marcelo J. Kuroda1

Divisions of 1 Immunology and 2 Comparative Pathology, Tulane National Primate Research Center, Tulane University Health Science Center, Covington, LA; 3 Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; and 4 Theoretical Biology and Biophysics, Los Alamos National Laboratory, NM

It is widely accepted that destruction of CD4+ T cells and viral load are the primary markers for immunodeficiency in HIV-1–infected humans and in simian immunodeficiency virus (SIV)–infected macaques. However, monocyte/macrophages are also important targets of HIV/SIV infection and a critical link between innate and adaptive immunity. We therefore examined whether changes in cells of the monocyte/macrophage lineage could be linked to the pathogenesis of AIDS in the rhesus macaque model. Here, we show that massive turnover of peripheral monocytes associated with death of tissue macrophages correlates with AIDS progression in macaques. More importantly, the level of monocyte turnover was not linked to the CD4+ T-cell count and was a better predictive marker for AIDS progression than was viral load or lymphocyte activation. Our results show the importance of monocyte/macrophages in the pathogenesis of AIDS and suggest the dynamic changes of the monocyte/macrophages as a new marker for AIDS progression.


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