Journal
JOURNAL OF VIROLOGY
Volume 74, Issue 23, Pages 11001-11007Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.74.23.11001-11007.2000
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Funding
- NCRR NIH HHS [K26 RR000168, P51 RR000168, RR00168] Funding Source: Medline
- NICHD NIH HHS [HD36310] Funding Source: Medline
- NIDDK NIH HHS [R01 DK050550, DK50550] Funding Source: Medline
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Early viral replication and profound CD4(+) T-cell depletion occur preferentially in intestinal tissues of macaques infected with simian immunodeficiency virus (SM. Here we show that a much higher percentage of CD4(+) T cells in the intestine express CCR5 compared with those found in the peripheral blood, spleen, or lymph nodes. In addition, the selectivity and extent of the CD4(+) T-cell loss in SIV infection may depend upon these cells coexpressing CCR5 and having a memory phenotype (CD45RA(-)). Following intravenous infection with SIVmac251, memory CD4(+) CCR5(+) T cells were selectively eliminated within 14 days in all major lymphoid tissues (intestine, spleen, and lymph nodes). However, the effect on CD4(+) T-cell numbers was most profound in the intestine, where cells of this phenotype predominate. The CD4(+) T cells that remain after 14 days of infection lacked CCR5 and/or were naive (CD45RA(+)). Furthermore, when animals in the terminal stages of SIV infection (with AIDS) were examined, virtually no CCR5-expressing CD4(+) T cells were found in lymphoid tissues, and all of the remaining CD4(+) T cells were naive and coexpressed CXCR4. These findings suggest that chemokine receptor usage determines which cells are targeted for SIV infection and elimination in vivo.
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