Human and simian immunodeficiency virus-infected chimpanzees do not have increased intracellular levels of β-chemokines in contrast to infected humans
✍ Scribed by Pascale Ondoa; Chris Vereecken; Katrien Fransen; Robert Colebunders; Guido van der Groen; Jonathan L. Heeney; Luc Kestens
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 181 KB
- Volume
- 69
- Category
- Article
- ISSN
- 0146-6615
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✦ Synopsis
Abstract
This study was undertaken to explain why chimpanzees infected with HIV‐1 (human immunodeficiency virus type 1) or SIV~cpz~ (simian immunodeficiency virus of chimpanzee) are relatively resistant to AIDS (acquired immunodeficiency syndrome). The numbers of β‐chemokine‐positive cells were compared between uninfected and infected humans and chimpanzees using three‐color cytofluorometry. In humans, the percentage of β‐chemokine‐positive cells was significantly higher in CD8^+^ T and natural killer (NK) cells than in CD4^+^ T cells in both uninfected and HIV‐1‐infected individuals. In the presence of HIV‐1 infection, however, both CD8^+^ and CD4^+^ T cell subsets contained significantly more β‐chemokine‐positive cells than in the absence of infection. Interestingly, in chimpanzees two important differences were noted. First, their percentage of β‐chemokine‐positive CD8^+^ T and NK cells was significantly higher than in uninfected humans. Second, in contrast to humans, infection with either HIV‐1 or with SIV~cpz~ was not associated with increased numbers of β‐chemokine‐positive cells. These results indicate that: constitutive high levels of intracellular β‐chemokines in chimpanzees' CD8 lymphocytes and NK cells do not necessarily correspond to lower levels of virus replication during the chronic phase of infection; and increased percentages of β‐chemokine‐positive cells in HIV‐infection are not a correlate of disease resistance. The data suggest that neither pre‐nor post‐exposure levels of intracellular β‐chemokines are correlated with the subsequent control of disease progression. J. Med. Virol. 69:297–305, 2003. © 2003 Wiley‐Liss, Inc.