CHARACTERIZATION OF A NEW SIV FROM AGILE MANGABEY (CERCOCEBUS AGILIS)

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 到目前为止，有两种芒果鱼被描述为存在SIV：黑头山竹(SIVsm)和红帽山竹(SIVrcm)。它们聚集在两个不同的谱系中。对从喀麦隆敏捷的芒果鱼中分离到的SIVagi进行了遗传学和生物学特性的研究，以研究慢病毒在芒果鱼中的进化。在喀麦隆巴斯德中心，用ELISA和Western Blot检测了10只圈养敏捷曼加比的血液中的抗SIV抗体。多肽EIA检测主要谱系的SIV的V3和gp36反应性。在Agilis PBMCs、人PBMCs和细胞系上进行病毒培养。调查共受体的使用情况，并进行CCR-5测序以调查受试猴子的Delta-24基因型。扩增了GAG和Pol基因片段，并进行了系统发育分析。10只猴子中有2只(20%)有抗体。多肽分析表明，两个样品的V3多肽和SIVrcm gp36都没有反应。其中一只猴子(703只)的培养呈阳性。该病毒株在人外周血单核细胞上生长。没有猕猴存在Delta-24碱基缺失。然而，SIVagiCam703使用CCR-2进行病毒进入，类似于SIVrcm。系统发育分析表明，在所分析的两个地区中，SIVagi在SIVrcm谱系中聚在一起。我们目前已经对包含LTR-Poll的4500个碱基进行了测序，进一步的分析正在进行中。灵敏的猴子天生就感染了一种独特的SIVagi。该病毒是从SIVrcm交叉传播的，这一点得到了系统发育分析的支持。这种跨物种传播似乎是最近的，因为交叉传播的病毒仍然使用Ccr-2共受体进入病毒，尽管Ccr-5 Delta-24在敏捷的芒果中频率很低。SIVagi代表了慢病毒多样性和致病机制之谜的新片段。有必要进行长期随访，以确定这种交叉传播病毒在灵敏猴子身上的致病潜力。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Two species of mangabeys were described to date to harbor SIVs: sooty mangabeys (SIVsm) and red-capped mangabeys (SIVrcm). They cluster in two different lineages. SIVagi isolated from agile mangabeys in Cameroon were philogenetically and biologically characterized in order to investigate the evolution of lentiviruses in mangabeys. Blood from 10 captive agile mangabeys was tested at Centre Pasteur Cameroon for anti-SIV antibody using ELISA and Western Blot. V3 and gp36 reactivity for SIVs from major lineages were tested by peptide EIA. Virus cultures were done on agilis PBMCs, human PBMCs and cell lines. Co-receptor use was investigated and CCR-5 sequencing was done to investigate delta-24 genotype of the tested monkeys. gag and pol fragments were amplified and phylogeneticly analyzed. Two out the ten monkeys (20%) had antibody. Peptide assays showed no reaction on the V3 peptides and SIVrcm gp36 reactivity for both samples. Cultures of one of these monkeys (703) were positive. This virus strain was grown on human PBMCs. No monkeys had the delta-24 bp deletion. However, SIVagiCam703 used CCR-2 for viral entry, similar to the SIVrcm. Phylogenetic analysis showed that SIVagi clusters within SIVrcm lineage in both analyzed regions. We have currently sequenced a 4,500 bp encompassing LTR-pol, and further analysis is in progress. Agile monkeys are naturally infected with a distinct SIVagi. This virus was cross-transmitted from SIVrcm, which is supported by phylogenetic analyses. This cross-species transmission seems to be recent, as the cross-transmitted virus still uses the CCR-2 co-receptor for virus entry, in spite of the low frequency of CCR-5 delta-24 in the agile mangabeys. SIVagi represent new piece in the puzzle of lentiviral diversity and pathogenesis. Long-term follow-up is necessary to characterize the pathogenic potential of this cross-transmitted virus in agile monkeys