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澳大利亚和欧洲的粘液瘤病:新兴传染病模型。

Myxomatosis in Australia and Europe: a model for emerging infectious diseases.

机构信息

CSIRO Ecosystem Sciences, GPO Box 1700, Canberra, ACT 2601, Australia.

出版信息

Antiviral Res. 2012 Mar;93(3):387-415. doi: 10.1016/j.antiviral.2012.01.009. Epub 2012 Feb 8.

DOI:10.1016/j.antiviral.2012.01.009
PMID:22333483
Abstract

Myxoma virus is a poxvirus naturally found in two American leporid (rabbit) species (Sylvilagus brasiliensis and Sylvilagus bachmani) in which it causes an innocuous localised cutaneous fibroma. However, in European rabbits (Oryctolagus cuniculus) the same virus causes the lethal disseminated disease myxomatosis. The introduction of myxoma virus into the European rabbit population in Australia in 1950 initiated the best known example of what happens when a novel pathogen jumps into a completely naïve new mammalian host species. The short generation time of the rabbit and their vast numbers in Australia meant evolution could be studied in real time. The carefully documented emergence of attenuated strains of virus that were more effectively transmitted by the mosquito vector and the subsequent selection of rabbits with genetic resistance to myxomatosis is the paradigm for pathogen virulence and host-pathogen coevolution. This natural experiment was repeated with the release of a separate strain of myxoma virus in France in 1952. The subsequent spread of the virus throughout Europe and its coevolution with the rabbit essentially paralleled what occurred in Australia. Detailed molecular studies on myxoma virus have dissected the role of virulence genes in the pathogenesis of myxomatosis and when combined with genomic data and reverse genetics should in future enable the understanding of the molecular evolution of the virus as it adapted to its new host. This review describes the natural history and evolution of myxoma virus together with the molecular biology and experimental pathogenesis studies that are informing our understanding of evolution of emerging diseases.

摘要

粘液瘤病毒是一种自然存在于两种美洲兔(Sylvilagus brasiliensis 和 Sylvilagus bachmani)中的痘病毒,在这些兔子中,它会引起无害的局部皮肤纤维瘤。然而,在欧洲兔(Oryctolagus cuniculus)中,同样的病毒会导致致命的弥散性疾病粘液瘤病。1950 年,粘液瘤病毒被引入澳大利亚的欧洲兔种群,这是一个著名的例子,说明了当一种新的病原体进入一个完全陌生的新哺乳动物宿主物种时会发生什么。兔子的短世代时间和它们在澳大利亚的大量存在意味着进化可以实时研究。经过精心记录的病毒减毒株的出现,这些病毒更容易通过蚊子媒介传播,以及随后对具有抗粘液瘤病遗传抗性的兔子的选择,这是病原体毒力和宿主-病原体共同进化的典范。1952 年,法国释放了另一种粘液瘤病毒,再次重复了这个自然实验。随后,病毒在整个欧洲的传播及其与兔子的共同进化基本上与澳大利亚发生的情况相同。对粘液瘤病毒的详细分子研究剖析了毒力基因在粘液瘤病发病机制中的作用,当与基因组数据和反向遗传学结合时,应该能够在未来理解病毒作为适应新宿主而发生的分子进化。这篇综述描述了粘液瘤病毒的自然历史和进化,以及分子生物学和实验发病机制研究,这些研究为我们理解新发疾病的进化提供了信息。

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