Concomitant Immunity and Worm Senescence May Drive Schistosomiasis Epidemiological Patterns: An Eco-Evolutionary Perspective

Concomitant Immunity and Worm Senescence May Drive Schistosomiasis Epidemiological Patterns: An Eco-Evolutionary Perspective
复制标题

DOI:
10.3389/fimmu.2020.00160
复制
发表时间:
2020-02-25
影响因子:
7.3
通讯作者:
Sokolow, Susanne H.
Sokolow, Susanne H.
中科院分区:
医学2区
文献类型:
--
作者:
Buck, Julia C.;De Leo, Giulio A.;Sokolow, Susanne H.

文献摘要

被引文献

相似文献

在人血吸虫病流行的地区,感染率和产蛋量在儿童期迅速上升,在8-15岁达到高峰,此后下降。一个类似的高峰(“过冲”),然后恢复到平衡感染水平,有时发生在大规模给药后一年或更短的时间。这些模式通常被认为是由于获得性免疫,这是由暴露引起的,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不同暴露、宿主的不同死亡率和进行性病理学。在这里,我们回顾这些解释,并提供了一个新的(但不相互排斥)的解释,即成虫保护主机对幼虫阶段为自己的利益(“伴随免疫”)和蠕虫的繁殖力下降蠕虫年龄(“生殖衰老”)。这种解释从生态进化的角度来看待血吸虫病,因为伴随的免疫通过减少宿主内的种内竞争来最大限度地提高蠕虫的适应性。如果是正确的,我们的假设可能对治疗和控制人类血吸虫病有深远的影响。具体来说,如果免疫是蠕虫导向的,那么治疗由年老衰老的蠕虫组成的长期感染可以使新的、繁殖力高的蠕虫感染成为可能。此外,我们的假设表明,重新研究治疗方法,模仿蠕虫的伴随免疫调节活性,同时尽量减少其卵的病理后果。我们强调宿主-寄生虫相互作用的生态进化观点的价值。
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.