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Concomitant Immunity and Worm Senescence May Drive Schistosomiasis Epidemiological Patterns: An Eco-Evolutionary Perspective.
Frontiers in Immunology ( IF 5.7 ) Pub Date : 2020-01-21 , DOI: 10.3389/fimmu.2020.00160
Julia C Buck 1 , Giulio A De Leo 2, 3 , Susanne H Sokolow 2, 3
Affiliation  

In areas where human schistosomiasis is endemic, infection prevalence and egg output are known to rise rapidly through childhood, reach a peak at 8–15 years of age, and decline thereafter. A similar peak (“overshoot”) followed by return to equilibrium infection levels sometimes occurs a year or less after mass drug administration. These patterns are usually assumed to be due to acquired immunity, which is induced by exposure, directed by the host's immune system, and develops slowly over the lifetime of the host. Other explanations that have been advanced previously include differential exposure of hosts, differential mortality of hosts, and progressive pathology. Here we review these explanations and offer a novel (but not mutually exclusive) explanation, namely that adult worms protect the host against larval stages for their own benefit (“concomitant immunity”) and that worm fecundity declines with worm age (“reproductive senescence”). This explanation approaches schistosomiasis from an eco-evolutionary perspective, as concomitant immunity maximizes the fitness of adult worms by reducing intraspecific competition within the host. If correct, our hypothesis could have profound implications for treatment and control of human schistosomiasis. Specifically, if immunity is worm-directed, then treatment of long-standing infections comprised of old senescent worms could enable infection with new, highly fecund worms. Furthermore, our hypothesis suggests revisiting research on therapeutics that mimic the concomitant immunity-modulating activity of adult worms, while minimizing pathological consequences of their eggs. We emphasize the value of an eco-evolutionary perspective on host-parasite interactions.



中文翻译:


伴随的免疫和蠕虫衰老可能会驱动血吸虫病的流行病学模式:生态进化的视角。



在人类血吸虫病流行的地区,感染率和产蛋量在儿童时期迅速上升,在 8-15 岁时达到顶峰,然后下降。有时,在大规模给药后一年或更短时间内,会出现类似的峰值(“过冲”),然后恢复到平衡感染水平。这些模式通常被认为是由于获得性免疫,这种免疫是由暴露引起的,由宿主的免疫系统指导,并在宿主的一生中缓慢发展。先前提出的其他解释包括宿主的差异暴露、宿主的差异死亡率和进行性病理学。在这里,我们回顾这些解释并提出一个新颖的(但不是相互排斥的)解释,即成虫为了自身利益而保护宿主免受幼虫阶段的侵害(“伴随免疫”),并且蠕虫的繁殖力随着蠕虫年龄的增长而下降(“生殖衰老”) )。这种解释从生态进化的角度来解释血吸虫病,因为伴随免疫通过减少宿主内的种内竞争来最大限度地提高成虫的适应性。如果正确,我们的假设可能会对人类血吸虫病的治疗和控制产生深远的影响。具体来说,如果免疫是针对蠕虫的,那么对由老衰老蠕虫组成的长期感染的治疗可能会导致新的、高繁殖力蠕虫的感染。此外,我们的假设建议重新审视模仿成虫伴随的免疫调节活性的疗法研究,同时最大限度地减少其卵的病理后果。我们强调生态进化视角对宿主与寄生虫相互作用的价值。

更新日期:2020-02-25
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