Schistosomes induce severe hepatic disease, which is fatal in 2-10% of cases, mortality being higher in cases of co-infection with HBV or HCV. Hepatic disease occurs as a consequence of the chronic inflammation caused by schistosome eggs trapped in liver sinusoids. In certain individuals, the repair process leads to a massive accumulation of fibrosis in the periportal spaces. We and others have shown that genetic variants play a crucial role in disease progression from mild to severe fibrosis and explain why hepatic fibrosis progresses rapidly in certain subjects only. We will review here published findings concerning the strategies that have been used in the analysis of hepatic fibrosis in schistosome-infected individuals, the genetic variants that have associated with fibrosis, and variants in new pathways crucial for fibrosis progression. Together, these studies show that the development of fibrosis is under the tight genetic control of various common variants with moderate effects. This polygenic control has made it possible to develop models that identify schistosome-infected individual at risk of severe hepatic disease. We discuss the performances and limitations of these models.

中文翻译：

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遗传算法可识别出由血吸虫引起的严重肝病高危人群。

血吸虫诱发严重的肝病，在2-10％的病例中致命，在HBV或HCV合并感染的情况下死亡率更高。肝病是由肝窦中捕获的血吸虫卵引起的慢性炎症的结果。在某些个体中，修复过程会导致在门静脉周围空间大量积聚纤维化。我们和其他人已经表明，遗传变异在从轻度到重度纤维化的疾病进展中起关键作用，并解释了为什么肝纤维化仅在某些受试者中快速发展。我们将在这里回顾已发表的发现，这些发现涉及在血吸虫感染的个体中分析肝纤维化所使用的策略，与纤维化相关的遗传变异以及对纤维化进展至关重要的新途径的变异。总之，这些研究表明，纤维化的发生在各种常见变体的严格遗传控制下，且具有中等作用。这种多基因对照使开发能够鉴定出患有严重肝病风险的血吸虫感染个体的模型成为可能。我们讨论了这些模型的性能和局限性。