Journal
JOURNAL OF VIROLOGY
Volume 74, Issue 3, Pages 1209-1223Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.74.3.1209-1223.2000
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Funding
- NCRR NIH HHS [P51 RR000165, P51 RR000164] Funding Source: Medline
- NIAID NIH HHS [R01 AI38573, P30 AI042848, R01 AI40387, R01 AI41945, R01 AI065310, R01 AI041945] Funding Source: Medline
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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 cu 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 al 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.
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