Apetrei Cristian, Gautam Rajeev, Sumpter Beth, Carter Anders C, Gaufin Thaidra, Staprans Silvija I, Else James, Barnes Mary, Cao Robert, Garg Seema, Milush Jeffrey M, Sodora Donald L, Pandrea Ivona, Silvestri Guido
Division of Microbiology and Immunology, Tulane National Primate Research Center, 18703 Three Rivers Road, Covington, LA 70433, USA.
J Virol. 2007 Aug;81(15):7913-23. doi: 10.1128/JVI.00281-07. Epub 2007 May 16.
Simian immunodeficiency virus (SIV) SIV(smm) naturally infects sooty mangabeys (SMs) and is the source virus of pathogenic infections with human immunodeficiency virus type 2 (HIV-2) and SIV(mac) of humans and macaques, respectively. In previous studies we characterized SIV(smm) diversity in naturally SIV-infected SMs and identified nine different phylogenetic subtypes whose genetic distances are similar to those reported for the different HIV-1 group M subtypes. Here we report that, within the colony of SMs housed at the Yerkes National Primate Research Center, at least four SIV(smm) subtypes cocirculate, with the vast majority of animals infected with SIV(smm) subtype 1, 2, or 3, resulting in the emergence of occasional recombinant forms. While SIV(smm)-infected SMs show a typically nonpathogenic course of infection, we have observed that different SIV(smm) subtypes are in fact associated with specific immunologic features. Notably, while subtypes 1, 2, and 3 are associated with a very benign course of infection and preservation of normal CD4+ T-cell counts, three out of four SMs infected with subtype 5 show a significant depletion of CD4+ T cells. The fact that virus replication in SMs infected with subtype 5 is similar to that in SMs infected with other SIV(smm) subtypes suggests that the subtype 5-associated CD4+ T-cell depletion is unlikely to simply reflect higher levels of virus-mediated direct killing of CD4+ T-cells. Taken together, this systematic analysis of the subtype-specific features of SIV(smm) infection in natural SM hosts identifies subtype-specific differences in the pathogenicity of SIV(smm) infection.
猴免疫缺陷病毒（SIV）SIV（smm）可自然感染乌黑白眉猴（SMs），分别是人类2型免疫缺陷病毒（HIV - 2）和人类及猕猴的SIV（mac）致病性感染的源病毒。在先前的研究中，我们对自然感染SIV的SMs中SIV（smm）的多样性进行了表征，并鉴定出九种不同的系统发育亚型，其遗传距离与报道的不同HIV - 1组M亚型的遗传距离相似。在此我们报告，在耶基斯国家灵长类动物研究中心饲养的SMs群体中，至少有四种SIV（smm）亚型同时传播，绝大多数动物感染的是SIV（smm）亚型1、2或3，偶尔会出现重组形式。虽然感染SIV（smm）的SMs显示出典型的非致病性感染过程，但我们观察到不同的SIV（smm）亚型实际上与特定的免疫特征相关。值得注意的是，虽然亚型1、2和3与非常良性的感染过程以及正常CD4 + T细胞计数的维持相关，但感染亚型5的四只SMs中有三只显示出CD4 + T细胞的显著耗竭。感染亚型5的SMs中的病毒复制与感染其他SIV（smm）亚型的SMs中的病毒复制相似，这一事实表明，与亚型5相关的CD4 + T细胞耗竭不太可能仅仅反映病毒介导的对CD4 + T细胞直接杀伤的更高水平。综上所述，对自然SM宿主中SIV（smm）感染的亚型特异性特征的这一系统分析确定了SIV（smm）感染致病性中的亚型特异性差异。
