Restrictions to cross-species transmission of lentiviral infection gleaned from studies of FIV.
Restrictions to cross-species transmission of lentiviral infection gleaned from studies of FIV.
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DOI：
10.1016/j.vetimm.2009.10.005
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发表时间：
2010-03-15
影响因子：
1.8
通讯作者：
Poss M
中科院分区：
文献类型：
--
作者：
VandeWoude S;Troyer J;Poss M
40多种灵长类动物和20多种猫含有对慢病毒抗原产生血清反应的抗体。在几乎所有进行了病毒基因分析的病例中，每个宿主物种都感染了一种独特的慢病毒。尽管慢病毒在一个物种内的分支可能有很大的分歧，但它们在该物种内通常是单系进化的。与这一观察结果明显不同的是，在南加州的山猫(Lynx Rufus)和美洲狮(Puma Concolor)之间，FIV明显的跨物种传播至少发生了三次；来自一个山猫序列的证据表明，这种交叉可能也发生在佛罗里达州山猫和濒危的佛罗里达州黑豹之间。其他几个孤立的报告表明，FIV分离株在近距离圈养动物中跨物种传播，众所周知，HIV-1和HIV-2来自人类与感染SIV的非人类灵长类动物的接触。通过一个实验模型，我们已经确定家猫(Felis Catus)对源于美洲狮或狮子的FIV易感。虽然感染最初是复制的，动物血清转换，但在相对较短的时间内，在大多数动物中传播的病毒减少到几乎检测不到的水平。病毒载量的这种减少与最初的病毒峰值成正比。虽然在胃肠道组织中可以发现病毒库，但大多数在外围恢复的病毒基因组都发生了高度突变，这表明非适应宿主成功地抑制了正常的病毒复制，导致了复制能力不强的病毒后代。在自然环境中，这种限制跨物种感染的可能机制包括：1.缺乏有利于不同物种的感染和脱落动物之间慢病毒传播的接触；2.缺乏适当的受体谱系，允许病毒进入新物种的敏感细胞；3.新宿主中的细胞机制与主要宿主足够不同，以支持病毒复制(即被动的、非促进的病毒复制)；4.新宿主中存在的能够限制病毒复制的细胞内限制机制(即主动的、中断的病毒复制)。这些因素包括限制脱壳、复制、包装和病毒粒子释放的因素；5.新宿主提高杀菌适应性免疫的独特能力，导致流产的感染，不能在同种之间传播感染；或6.产生缺陷或非传染性的病毒后代，缺乏使其对同种物质具有传染性的细胞辅助因子(即，在病毒环境中缺乏适当的细胞成分的颗粒，使其对同一物种的其他动物具有传染性)。本综述描述了支持或反驳这些可能性的相对重要性的数据。基于我们体内跨物种模型的见解表明，细胞内限制机制有效地抑制了慢病毒在物种间的快速传播。此外，自然种群中物种内部和物种之间有限的接触与限制FIV毒株传播的机会高度相关。对自然产生的SIV和先天宿主限制系统的研究表明，这两种机制也是抑制慢病毒在灵长类物种中跨物种广泛传播的重要因素。
More than 40 species of primates and over 20 species of cats harbor antibodies that sero-react to lentiviral antigens. In nearly all cases where viral genetic analysis has been conducted, each host species is infected with a unique lentivirus. Though lentivirus clades within a species can be substantially divergent, they are typically monophyletic within that species. A notable significant departure from this observation is apparent cross-species transmission of FIV between bobcats (Lynx rufus) and pumas (Puma concolor) in southern California that has occurred at least three times; evidence from one bobcat sequence suggests this cross-over may have also occurred in Florida between bobcats and the endangered Florida panther. Several other isolated reports demonstrate cross-species transmission of FIV isolates among captive animals housed in close proximity, and it is well established that HIV-1 and HIV-2 arose from human contact with SIV-infected nonhuman primates. Using an experimental model, we have determined that domestic cats (Felis catus) are susceptible to FIVs originating from pumas or lions. While infections are initially replicative, and animals seroconvert, within a relatively short period of time circulating virus is reduced to nearly undetectable levels in a majority of animals. This diminution of viral load is proportional to initial viral peak. Although viral reservoirs can be identified in gastrointestinal tissues, most viral genomes recovered peripherally are highly mutated, suggesting that the non-adapted host successfully inhibits normal viral replication, leading to replication incompetent viral progeny. Mechanisms possible for such restriction of cross-species infections in natural settings include: 1. Lack of contact conducive to lentiviral transmission between infected and shedding animals of different species; 2. Lack of suitable receptor repertoire to allow viral entry to susceptible cells of a new species; 3. Cellular machinery in the new host sufficiently divergent from the primary host to support viral replication (ie passive unfacilitated viral replication); 4. Intracellular restriction mechanisms present in the new host that is able to limit viral replication (i.e. active interrupted viral replication. These include factors that limit uncoating, replication, packaging, and virion release); 5. Unique ability of new host to raise sterilizing adaptive immunity, resulting in aborted infection and inability to spread infections among con-specifics; or, 6. Production of defective or non-infectious viral progeny that lack cellular cofactors to render them infectious to conspecifics (i.e. particles lacking appropriate cellular components in viral Env to render them infectious to other animals of the same species). Data to support or refute the relative importance of each of these possibilities is described in this review. Insights based on our in vivo cross-species model suggest intracellular restriction mechanisms effectively inhibit rapid inter-specific transmission of lentiviruses. Further, limited contact both within and between species in natural populations is highly relevant to limiting the opportunity for spread of FIV strains. Studies of naturally-occurring SIV and innate host restriction systems suggest these same two mechanisms are significant factors inhibiting widespread cross-species transmission of lentiviruses among primate species as well.
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影响因子：
5.4
作者：
Chen, ZW;Luckay, A;Marx, PA
通讯作者：
Marx, PA
影响因子：
5.4
作者：
Hatch, Steven C.;Archer, Jacob;Gummuluru, Suryaram
通讯作者：
Gummuluru, Suryaram
影响因子：
0.7
作者：
GOLDSTEIN, S;ELKINS, WR;HIRSCH, VM
通讯作者：
HIRSCH, VM
DOI：
10.1073/pnas.0812587106
发表时间：
2009-03-17
影响因子：
11.1
作者：
Hatziioannou, Theodora;Ambrose, Zandrea;Bieniasz, Paul D.
通讯作者：
Bieniasz, Paul D.
影响因子：
1.5
作者：
CRANAGE, MP;POLYANSKAYA, N;FARRAR, GH
通讯作者：
FARRAR, GH