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Updated: Aug 15, 2026
Cercarial Transformation and in vitro Cultivation of Schistosoma mansoni Schistosomules
Published on: August 16, 2011
Complement C2 receptor inhibitor trispanning: from man to schistosome
1Immunonephrology, Department of Research, University Hospital Basel, Basel, Switzerland. jameel.inal@unibas.ch
Insights
Horizontal gene transfer (HGT) may explain how the CRIT gene, found in humans and parasites like Schistosoma, evolved. This genetic transfer between hosts and parasites is a poorly understood but significant evolutionary mechanism.
Area of Science:
- Genetics
- Evolutionary Biology
- Parasitology
Background:
- The complement inhibitor CRIT was initially identified in human parasites like Schistosoma and Trypanosoma cruzi.
- CRIT gene distribution spans diverse species, including fish, rodents, and humans, suggesting a broader evolutionary role.
Purpose of the Study:
- To investigate the evolutionary origins of the CRIT gene in humans and parasites.
- To test the hypothesis of host-to-parasite horizontal gene transfer (HGT) as the mechanism for CRIT acquisition in schistosomes.
Main Methods:
- Phylogenetic analysis of CRIT genes at the nucleotide level to assess evolutionary distances.
- Comparative analysis of CRIT gene function, protein structure, and genomic organization between species.
Main Results:
- Phylogenetic analysis revealed significant evolutionary proximity between human and Schistosoma CRIT genes.
- Identical function, high nucleotide/amino acid identity, and similar secondary protein structures were observed for CRIT across species.
- Genomic organization of CRIT was found to be identical between human and schistosome parasites.
Conclusions:
- The data strongly support the hypothesis that CRIT in humans and schistosomes is orthologous.
- Host-to-parasite HGT is proposed as the likely mechanism for the presence of CRIT in schistosomes.
- This study highlights HGT as a significant, yet under-described, factor in host-parasite co-evolution.
Abstract:
Horizontal gene transfer (HGT), in relation to genetic transfer between hosts and parasites, is a little described mechanism. Since the complement inhibitor CRIT was first discovered in the human Schistosoma parasite (the causative agent of Bilharzia) and in Trypanosoma cruzi (a parasite causing Chagas' disease), it has been found to be distributed amongst various species, ranging from the early teleost cod to rats and humans. In terms of evolutionary distance, as measured in a phylogenetic analysis of these CRIT genes at nucleotide level, the parasitic species are as removed from their human host as is the rat sequence, suggesting HGT. The hypotheses that CRIT in humans and schistosomes is orthologous and that the presence of CRIT in schistosomes occurs as a result of host-to-parasite HGT are presented in the light of empirical data and the growing body of data on mobile genetic elements in human and schistosome genomes. In summary, these data indicate phylogenetic proximity between Schistosoma and human CRIT, identity of function, high nucleotide/amino acid identity and secondary protein structure, as well as identical genomic organization.
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