Pandrea Ivona, Apetrei Cristian, Gordon Shari, Barbercheck Joseph, Dufour Jason, Bohm Rudolf, Sumpter Beth, Roques Pierre, Marx Preston A, Hirsch Vanessa M, Kaur Amitinder, Lackner Andrew A, Veazey Ronald S, Silvestri Guido
Tulane National Primate Research Center, Covington, LA 70433, USA.
Blood. 2007 Feb 1;109(3):1069-76. doi: 10.1182/blood-2006-05-024364. Epub 2006 Sep 26.
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 nonnatural/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.
与人类和猕猴的慢病毒感染不同，天然宿主感染猿猴免疫缺陷病毒（SIV）时，尽管病毒复制水平很高，但却不具有致病性。然而，这种无疾病状态背后的机制尚不清楚。在此我们报告，从血液、淋巴结和黏膜组织分离出的CD4+ T细胞上，SIV感染的天然宿主表达的CCR5水平极低。鉴于在5种不同的天然SIV宿主物种（乌黑白眉猴、非洲绿猴、山魈、太阳尾猴和黑猩猩）中发现了这种免疫特征，而在5种非天然/近期宿主（人类、恒河猴、猪尾猴、食蟹猴和狒狒）中却不存在，它可能代表了病毒与其天然宿主共同进化导致非致病性感染的一个关键特征。CD4+ T细胞上低水平CCR5表达的有益作用可能包括减少病毒复制的靶细胞以及减少活化的CD4+ T细胞向炎症组织的归巢。
