Kerr Peter J, Liu June, Cattadori Isabella, Ghedin Elodie, Read Andrew F, Holmes Edward C
CSIRO Biosecurity Flagship, Black Mountain Laboratories, Clunies Ross Street, Acton, ACT 2601, Australia.
Center for Infectious Disease Dynamics, Department of Biology, The Pennsylvania State University, University Park, PA 16802, USA.
Viruses. 2015 Mar 6;7(3):1020-61. doi: 10.3390/v7031020.
Myxoma virus (MYXV) is the type species of the Leporipoxviruses, a genus of Chordopoxvirinae, double stranded DNA viruses, whose members infect leporids and squirrels, inducing cutaneous fibromas from which virus is mechanically transmitted by biting arthropods. However, in the European rabbit (Oryctolagus cuniculus), MYXV causes the lethal disease myxomatosis. The release of MYXV as a biological control for the wild European rabbit population in Australia, initiated one of the great experiments in evolution. The subsequent coevolution of MYXV and rabbits is a classic example of natural selection acting on virulence as a pathogen adapts to a novel host species. Slightly attenuated mutants of the progenitor virus were more readily transmitted by the mosquito vector because the infected rabbit survived longer, while highly attenuated viruses could be controlled by the rabbit immune response. As a consequence, moderately attenuated viruses came to dominate. This evolution of the virus was accompanied by selection for genetic resistance in the wild rabbit population, which may have created an ongoing co-evolutionary dynamic between resistance and virulence for efficient transmission. This natural experiment was repeated on a continental scale with the release of a separate strain of MYXV in France and its subsequent spread throughout Europe. The selection of attenuated strains of virus and resistant rabbits mirrored the experience in Australia in a very different environment, albeit with somewhat different rates. Genome sequencing of the progenitor virus and the early radiation, as well as those from the 1990s in Australia and Europe, has shown that although MYXV evolved at high rates there was no conserved route to attenuation or back to virulence. In contrast, it seems that these relatively large viral genomes have the flexibility for multiple pathways that converge on a similar phenotype.
黏液瘤病毒(MYXV)是兔痘病毒属的模式种,兔痘病毒属属于痘病毒亚科,是双链DNA病毒,其成员感染兔科动物和松鼠,引发皮肤纤维瘤,病毒通过叮咬节肢动物进行机械传播。然而,在欧洲兔(穴兔)中,MYXV会引发致命疾病黏液瘤病。在澳大利亚,释放MYXV作为对野生欧洲兔种群的生物控制手段,开启了一项伟大的进化实验。随后,MYXV与兔子的共同进化是自然选择作用于毒力的经典例子,因为病原体适应了新的宿主物种。祖病毒的轻度减毒突变体更容易通过蚊子媒介传播,因为被感染的兔子存活时间更长,而高度减毒的病毒则可被兔子的免疫反应控制。因此,中度减毒的病毒开始占据主导地位。病毒的这种进化伴随着对野兔种群遗传抗性的选择,这可能在抗性和毒力之间形成了一种持续的共同进化动态,以实现有效传播。在法国释放另一株MYXV并随后在欧洲传播,在大陆规模上重复了这一自然实验。病毒减毒株和抗性兔子的选择反映了在澳大利亚截然不同的环境中的经历,尽管速度有所不同。对祖病毒及其早期辐射株,以及20世纪90年代澳大利亚和欧洲毒株的基因组测序表明,尽管MYXV进化速度很快,但不存在减毒或恢复毒力的保守途径。相反,似乎这些相对较大的病毒基因组具有多种途径的灵活性,这些途径汇聚到相似的表型上。