Abstract

Liver fibrosis is a wound-healing process purposely aimed at restoring organ integrity after severe injury caused by autoimmune reactions, mechanical stress or infections. The uncontrolled solicitation of this process is pathogenic and a pathognomonic feature of diseases like hepatosplenic schistosomiasis where exacerbated liver fibrosis is centrally positioned among the drivers of the disease morbidity and mortality. Intriguingly, however, liver fibrosis occurs and progresses dissimilarly in schistosomiasis-diseased individuals with the same egg burden and biosocial features including age, duration of residence in the endemic site and gender. This suggests that parasite-independent and currently poorly defined host intrinsic factors might play a defining role in the regulation of liver fibrosis, the hallmark of morbidity, during schistosomiasis. In this review, we therefore provide a comprehensive overview of all known host candidate regulators of liver fibrosis reported in the context of human schistosomiasis.

Highlights

  • Schistosomiasis represents the second most important parasitic disease in the world in terms of public health impact [1]

  • While Schistosoma haematobium adult worms reside in vessels of the bladder causing urinary schistosomiasis, those of Schistosoma mansoni and Schistosoma japonicum reside in the mesenteric veins of the intestinal tract causing hepatosplenic schistosomiasis leading to progressive liver fibrosis and portal hypertension [6]

  • Dessein et al in a primary study reported that several single nucleotide polymorphism (SNP) that lie close to the Connective Tissue Growth Factor (CTGF) gene are associated with severe hepatic fibrosis in individuals affected by hepatosplenic schistosomiasis [39, 60]

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Summary

Introduction

Schistosomiasis represents the second most important parasitic disease in the world in terms of public health impact [1]. In the context of hepatosplenic schistosomiasis, an accumulating number of studies have reported disparities between prevalence of infection and levels of tissue morbidity, characterized by the stage of advancement of hepatic fibrosis and the presence/absence of periportal fibrosis [11, 27,28,29,30].

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