Rey-Cuillé M A, Berthier J L, Bomsel-Demontoy M C, Chaduc Y, Montagnier L, Hovanessian A G, Chakrabarti L A
Virologie et Immunologie Cellulaire, Institut Pasteur, Paris, France.
J Virol. 1998 May;72(5):3872-86. doi: 10.1128/JVI.72.5.3872-3886.1998.
A serologic survey of primates living in a French zoo allowed identification of three cases of infection with simian immunodeficiency virus in sooty mangabeys (Cercocebus atys) (SIVsm). Viral isolates, which were designated SIVsmFr66, SIVsmFr74, and SIVsmFr85, were obtained after short-term culture of mangabey lymphoid cells. Phylogenetic analysis of gag and env sequences amplified directly from mangabey tissues showed that the three SIVsmFr were genetically close and that they constituted a new subtype within the diverse SIVsm-SIVmac-human immunodeficiency virus type 2 (HIV-2) group. We could reconstruct the transmission events that likely occurred in 1986 between the three animals and evaluate the divergence of SIVsmFr sequences since transmission. The estimated rate of mutation fixation was 6 x 10(-3) substitutions per site per year, which was as high as the rate found for SIVmac infection in macaques. These data indicated that SIVsmFr replicated at a high rate in mangabeys, despite the nonpathogenic character of infection in this host. The viral load evaluated by competitive PCR reached 20,000 viral DNA copies per 10(6) lymph node cells. In addition, productively infected cells were readily detected in mangabey lymphoid tissues by in situ hybridization. The amounts of viral RNA in plasma ranged from 10(5) to 10(7) copies per ml. The cell-associated and plasma viral loads were as high as those seen in susceptible hosts (humans or macaques) during the asymptomatic stage of HIV or SIVmac infections. Thus, the lack of pathogenicity of SIVsm for its natural host cannot be explained by limited viral replication or by tight containment of viral production.
对生活在法国一家动物园的灵长类动物进行的血清学调查发现，三只乌黑白眉猴（Cercocebus atys）感染了猴免疫缺陷病毒（SIVsm）。从白眉猴淋巴样细胞进行短期培养后获得了病毒分离株，分别命名为SIVsmFr66、SIVsmFr74和SIVsmFr85。对白眉猴组织中直接扩增的gag和env序列进行系统发育分析表明，这三种SIVsmFr在基因上相近，并且在多样的SIVsm-SIVmac-2型人类免疫缺陷病毒（HIV-2）组内构成一个新的亚型。我们能够重建1986年这三只动物之间可能发生的传播事件，并评估自传播以来SIVsmFr序列的分歧。估计的突变固定率为每年每个位点6×10⁻³个替换，这与猕猴中SIVmac感染的速率一样高。这些数据表明，尽管SIVsm在该宿主中的感染无致病性，但SIVsmFr在白眉猴中以高速度复制。通过竞争性PCR评估的病毒载量达到每10⁶个淋巴结细胞20,000个病毒DNA拷贝。此外，通过原位杂交在白眉猴淋巴样组织中很容易检测到有生产性感染的细胞。血浆中的病毒RNA量为每毫升10⁵至10⁷个拷贝。细胞相关和血浆病毒载量与HIV或SIVmac感染无症状期易感宿主（人类或猕猴）中的病毒载量一样高。因此，SIVsm对其天然宿主缺乏致病性不能用病毒复制受限或病毒产生的严格控制来解释。
