Apetrei Cristian, Robertson David L, Marx Preston A
Microbiology Division, Tulane National Primate Research Center, Covington, LA 40433, USA.
Front Biosci. 2004 Jan 1;9:225-54. doi: 10.2741/1154.
Simian immunodeficiency virus (SIV) naturally infects non-human primates in Africa. To date, 40 SIVs have been described both in natural hosts and in heterologous species. These viruses are highly diverse and the majority cluster in 6 relatively equidistant phylogenetic lineages. At least 8 SIVs are currently considered as recombinant viruses, based on different clustering patterns in different genomic regions. Only three types of genomes are known, based on the number of accessory genes: vpr-containing genomes, vpr-vpx containing genomes and vpr-vpu-containing genomes. vpx resulted by a duplication of the vpr gene following non-homologous recombination and is characteristic of SIVs infecting the Papionini tribe of monkeys and HIV-2 in humans. vpu is characteristic of SIVcpz and HIV-1 and may have originated from a recombination involving SIVs from cercopitecini monkeys. SIV seems to be non-pathogenic in the vast majority of natural hosts in spite of a high levels of viral replication. This is probably a consequence of virus-host adaptation, in which the incubation period of the disease generally exceeds the life span of the African primate host. SIVs also have a high propensity for cross-species transmission. In the new host, the outcome may vary from inapparent infection to highly pathogenic, the former being reported for African monkeys, whereas the latter being observed in macaques and humans. The high diversity of SIVs was generated by a high mutation rate due to a low fidelity of the reverse-transcriptase and active viral and host cell turnover, host-dependent evolution and recombination. Cross-species transmission is not rare, however preferential host switching may drive the majority of cross-species transmissions. Numerous SIVs tested so far are able to grow in vitro on human PBMC, therefore it has been postulated that SIV represents a threat for infection of humans in Central Africa and that AIDS is a zoonosis. However, although the simian origin of the two HIV types is broadly acknowledged, there are no data that AIDS is acquired like a zoonosis. SIV may undergo adaptation in the new human host in order to emerge in the general population. The study of SIV in their natural hosts should provide important clues to the real threat to human populations and also elucidate the mechanisms associated with a long-term persistent viral infection without clinical consequences for the host.
猿猴免疫缺陷病毒（SIV）自然感染非洲的非人灵长类动物。迄今为止，已在自然宿主和异种动物中发现了40种SIV。这些病毒高度多样化，大多数聚集在6个相对等距的系统发育谱系中。基于不同基因组区域的不同聚类模式，目前至少有8种SIV被认为是重组病毒。根据辅助基因的数量，已知只有三种类型的基因组：含vpr的基因组、含vpr-vpx的基因组和含vpr-vpu的基因组。vpx是vpr基因通过非同源重组复制产生的，是感染猴科狒狒族的SIV和人类HIV-2的特征。vpu是SIVcpz和HIV-1的特征，可能起源于涉及猕猴科猴子的SIV的重组。尽管病毒复制水平很高，但SIV在绝大多数自然宿主中似乎没有致病性。这可能是病毒-宿主适应性的结果，其中疾病的潜伏期通常超过非洲灵长类宿主的寿命。SIV也具有很高的跨物种传播倾向。在新宿主中，结果可能从不明显感染到高致病性不等，前者在非洲猴子中报道过，而后者在猕猴和人类中观察到。SIV的高度多样性是由逆转录酶的低保真性、活跃的病毒和宿主细胞更新、宿主依赖性进化和重组导致的高突变率产生的。跨物种传播并不罕见，然而，优先宿主转换可能推动了大多数跨物种传播。到目前为止，许多测试的SIV能够在人外周血单核细胞上体外生长，因此有人推测SIV对中非人类感染构成威胁，并且艾滋病是一种人畜共患病。然而，尽管两种HIV类型的猿猴起源已被广泛认可，但没有数据表明艾滋病是像人畜共患病那样获得的。SIV可能会在新的人类宿主中发生适应性变化，以便在普通人群中出现。对其自然宿主中的SIV进行研究应该为对人类种群的真正威胁提供重要线索，也阐明与长期持续病毒感染而对宿主没有临床后果相关的机制。
