Cattadori Isabella M, Albert Réka, Boag Brian
Division of Animal Production and Public Health, Faculty of Veterinary Medicine, The University of Glasgow, Glasgow G61 1QH, UK.
J R Soc Interface. 2007 Oct 22;4(16):831-40. doi: 10.1098/rsif.2007.1075.
One of the conditions that can affect host susceptibility and parasite transmission is the occurrence of concomitant infections. Parasites interact directly or indirectly within an individual host and often these interactions are modulated by the host immune response. We used a free-living rabbit population co-infected with the nematode Trichostrongylus retortaeformis, which appears to stimulate an acquired immune response, and the immunosuppressive poxvirus myxoma. Modelling was used to examine how myxoma infection alters the immune-mediated establishment and death/expulsion of T. retortaeformis, and consequently affects parasite intensity and duration of the infection. Simulations were based on the general TH1-TH2 immunological paradigm that proposes the polarization of the host immune response towards one of the two subsets of T helper cells. Our findings suggest that myxoma infections contribute to alter host susceptibility to the nematode, as co-infected rabbits showed higher worm intensity compared with virus negative hosts. Results also suggest that myxoma disrupts the ability of the host to clear T. retortaeformis as worm intensities were consistently high and remained high in old rabbits. However, the co-infection model has to include some immune-mediated nematode regulation to be consistent with field data, indicating that the TH1-TH2 dichotomy is not complete. We conclude that seasonal myxoma outbreaks enhance host susceptibility to the nematode and generate highly infected hosts that remain infectious for a longer time. Finally, the virus-nematode co-infection increases heterogeneities among individuals and potentially has a large effect on parasite transmission.
能够影响宿主易感性和寄生虫传播的条件之一是合并感染的发生。寄生虫在单个宿主体内直接或间接相互作用,而这些相互作用通常受到宿主免疫反应的调节。我们利用了一个自由生活的兔群,它们同时感染了似乎能刺激获得性免疫反应的线虫捻转血矛线虫和具有免疫抑制作用的痘病毒黏液瘤病毒。我们使用建模来研究黏液瘤病毒感染如何改变免疫介导的捻转血矛线虫的建立、死亡/排出,从而影响寄生虫强度和感染持续时间。模拟基于一般的TH1-TH2免疫范式,该范式提出宿主免疫反应向辅助性T细胞两个亚群之一极化。我们的研究结果表明,黏液瘤病毒感染导致宿主对该线虫的易感性发生改变,因为与病毒阴性宿主相比,合并感染的兔子体内线虫强度更高。结果还表明,黏液瘤病毒破坏了宿主清除捻转血矛线虫的能力,因为老年兔子体内的线虫强度一直很高且居高不下。然而,合并感染模型必须纳入一些免疫介导的线虫调节机制,才能与现场数据相符,这表明TH1-TH2二分法并不完整。我们得出结论,季节性的黏液瘤病毒爆发增强了宿主对该线虫 的易感性,并产生了感染程度高且感染期更长的宿主。最后,病毒-线虫合并感染增加了个体间的异质性,并可能对寄生虫传播产生重大影响。