Journal
BLOOD
Volume 109, Issue 3, Pages 1069-1076Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2006-05-024364
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Funding
- NCRR NIH HHS [P51 RR000165, RR00165, RR00164, P51 RR000164] Funding Source: Medline
- NIAID NIH HHS [R01 AI049809, R01 AI65325, R01 AI064066, R01 AI49080, R01 AI066998, R01 AI52755, R37 AI066998, AI66998, R01 AI64066, R01 AI49809, R01 AI065325, R01 AI052755, R01 AI049080] Funding Source: Medline
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In contrast to lentiviral infections of humans and macaques, simian immunodeficiency virus (SIV) infection of natural hosts is nonpathogenic despite high levels of viral replication. However, the mechanisms underlying this absence of disease are unknown. Here we report that natural hosts for SIV infection express remarkably low levels of CCR5 on CD4(+) T cells isolated from blood, lymph nodes, and mucosal tissues. Given that this immunologic feature is found in 5 different species of natural SIV hosts (sooty mangabeys, African green monkeys, mandrills, sun-tailed monkeys, and chimpanzees) but is absent in 5 normatural/recent hosts (humans, rhesus, pigtail, cynomolgus macaques, and baboons), it may represent a key feature of the coevolution between the virus and its natural hosts that led to a nonpathogenic infection. Beneficial effects of low CCR5 expression on CD4(+) T cells may include the reduction of target cells for viral replication and a decreased homing of activated CD4(+) T cells to inflamed tissue.
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