Tomasini Nicolás, Ragone Paula Gabriela, Gourbière Sébastien, Aparicio Juan Pablo, Diosque Patricio
Instituto de Patología Experimental, Facultad de Ciencias de la Salud, CONICET, Universidad Nacional de Salta, Salta, Argentina.
UMR 228 ESPACE-DEV-IMAGES, 'Institut de Modélisation et d'Analyses en Géo-Environnement et Santé', Université de Perpignan Via Domitia, Perpignan, France.
PLoS Comput Biol. 2017 May 8;13(5):e1005532. doi: 10.1371/journal.pcbi.1005532. eCollection 2017 May.
People living in areas with active vector-borne transmission of Chagas disease have multiple contacts with its causative agent, Trypanosoma cruzi. Reinfections by T. cruzi are possible at least in animal models leading to lower or even hardly detectable parasitaemia. In humans, although reinfections are thought to have major public health implications by increasing the risk of chronic manifestations of the disease, there is little quantitative knowledge about their frequency and the timing of parasite re-inoculation in the course of the disease. Here, we implemented stochastic agent-based models i) to estimate the rate of re-inoculation in humans and ii) to assess how frequent are reinfections during the acute and chronic stages of the disease according to alternative hypotheses on the adaptive immune response following a primary infection. By using a hybrid genetic algorithm, the models were fitted to epidemiological data of Argentinean rural villages where mixed infections by different genotypes of T. cruzi reach 56% in humans. To explain this percentage, the best model predicted 0.032 (0.008-0.042) annual reinfections per individual with 98.4% of them occurring in the chronic phase. In addition, the parasite escapes to the adaptive immune response mounted after the primary infection in at least 20% of the events of re-inoculation. With these low annual rates, the risks of reinfection during the typically long chronic stage of the disease stand around 14% (4%-18%) and 60% (21%-70%) after 5 and 30 years, with most individuals being re-infected 1-3 times overall. These low rates are better explained by the weak efficiency of the stercorarian mode of transmission than a highly efficient adaptive immune response. Those estimates are of particular interest for vaccine development and for our understanding of the higher risk of chronic disease manifestations suffered by infected people living in endemic areas.
生活在恰加斯病媒介传播活跃地区的人们会多次接触其病原体克氏锥虫。至少在动物模型中,克氏锥虫再次感染是可能的,这会导致较低甚至几乎检测不到的寄生虫血症。在人类中,尽管再次感染被认为通过增加疾病慢性表现的风险而对公共卫生具有重大影响,但关于其频率以及疾病过程中寄生虫再次接种的时间,定量知识却很少。在此,我们实施了基于主体的随机模型,一是为了估计人类的再次接种率,二是根据初次感染后适应性免疫反应的替代假设,评估疾病急性和慢性阶段再次感染的频率。通过使用混合遗传算法,这些模型被拟合到阿根廷农村村庄的流行病学数据,在这些村庄中,人类感染不同基因型克氏锥虫的混合感染率达到56%。为了解释这一百分比,最佳模型预测每人每年有0.032(0.008 - 0.042)次再次感染,其中98.4%发生在慢性期。此外,在至少20%的再次接种事件中,寄生虫能够逃避初次感染后产生的适应性免疫反应。由于每年的再次感染率较低,在疾病通常较长的慢性阶段,5年和30年后再次感染的风险分别约为14%(4% - 18%)和60%(21% - 70%),大多数个体总体上会被再次感染1 - 3次。与高效的适应性免疫反应相比,粪口传播模式效率低下更能解释这些低感染率。这些估计对于疫苗开发以及我们理解生活在流行地区的感染者患慢性病表现的较高风险尤为重要。