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Journal of Virology, February 2000, p. 1209-1223, Vol. 74, No. 3
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Normal T-Cell Turnover in Sooty Mangabeys Harboring Active Simian Immunodeficiency Virus Infection

Lisa A. Chakrabarti,1,* Sharon R. Lewin,1 Linqi Zhang,1 Agegnehu Gettie,1 Amara Luckay,1 Louis N. Martin,2 Eva Skulsky,1 David D. Ho,1 Cecilia Cheng-Mayer,1 and Preston A. Marx1,2,3

Aaron Diamond AIDS Research Center, The Rockefeller University, New York, New York,1 and Tulane Regional Primate Research Center, Tulane University Medical Center, Covington,2 and Department of Tropical Medicine, Tulane University, New Orleans,3 Louisiana

Received 26 August 1999/Accepted 2 November 1999

Sooty mangabeys naturally infected with simian immunodeficiency virus (SIV) remain healthy though they harbor viral loads comparable to those in rhesus macaques that progress to AIDS. To assess the immunologic basis of disease resistance in mangabeys, we compared the effect of SIV infection on T-cell regeneration in both monkey species. Measurement of the proliferation marker Ki-67 by flow cytometry showed that mangabeys harbored proliferating T cells at a level of 3 to 4% in peripheral blood irrespective of their infection status. In contrast, rhesus macaques demonstrated a naturally high fraction of proliferating T cells (7%) that increased two- to threefold following SIV infection. Ki-67+ T cells were predominantly CD45RA-, indicating increased proliferation of memory cells in macaques. Quantitation of an episomal DNA product of T-cell receptor alpha  rearrangement (termed alpha 1 circle) showed that the concentration of recent thymic emigrants in blood decreased with age over a 2-log unit range in both monkey species, consistent with age-related thymic involution. SIV infection caused a limited decrease of alpha 1 circle numbers in mangabeys as well as in macaques. Dilution of alpha 1 circles by T-cell proliferation likely contributed to this decrease, since alpha 1 circle numbers and Ki-67+ fractions correlated negatively. These findings are compatible with immune exhaustion mediated by abnormal T-cell proliferation, rather than with early thymic failure, in SIV-infected macaques. Normal T-cell turnover in SIV-infected mangabeys provides an explanation for the long-term maintenance of a functional immune system in these hosts.

* Corresponding author. Mailing address: Aaron Diamond AIDS Research Center, 455 First Ave., 6th Floor, New York, NY 10016. Phone: (212) 448-5043. Fax: (212) 725-1126. E-mail: chakra{at}adarc.org.

Journal of Virology, February 2000, p. 1209-1223, Vol. 74, No. 3
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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