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Published on: April 5, 2015
Invasion pathways and malaria severity in Kenyan Plasmodium falciparum clinical isolates
Anne-Marie Deans1, Susana Nery, David J Conway
1Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, Ashworth Laboratories, King's Buildings, West Mains Road, Edinburgh, UK.
Abstract:
The invasion of erythrocytes by Plasmodium falciparum occurs through multiple pathways that can be studied in vitro by examining the invasion of erythrocytes treated with enzymes such as neuraminidase, trypsin, and chymotrypsin. We have studied the invasion pathways used by 31 Kenyan P. falciparum isolates from children with uncomplicated or severe malaria. Six distinct invasion profiles were detected, out of eight possible profiles. The majority of isolates (23 of 31) showed neuraminidase-resistant, trypsin-sensitive invasion, characteristic of the pathway mediated by an unknown parasite ligand and erythrocyte receptor "X." The neuraminidase-sensitive, trypsin-sensitive phenotype consistent with invasion mediated by the binding of parasite ligand erythrocyte binding antigen 175 to glycophorin A, the most common invasion profile in a previous study of Gambian field isolates, was seen in only 3 of 31 Kenyan isolates. No particular invasion profile was associated with severe P. falciparum malaria, and there was no significant difference in the levels of inhibition by the various enzyme treatments between isolates from children with severe malaria and those from children with uncomplicated malaria (P, >0.1 for all enzymes; Mann-Whitney U test). These results do not support the hypothesis that differences in invasion phenotypes play an important role in malaria virulence and indicate that considerable gaps remain in our knowledge of the molecular basis of invasion pathways in natural P. falciparum infections.
Insights
Plasmodium falciparum malaria invasion pathways vary among Kenyan children. Most isolates used a neuraminidase-resistant pathway, unlike previous findings, and no pathway linked to severe malaria.
Area of Science:
- Malariology
- Molecular Parasitology
- Infectious Diseases
Background:
- Plasmodium falciparum invades human erythrocytes via multiple pathways.
- Understanding these invasion pathways is crucial for malaria control.
- Enzyme treatment of erythrocytes in vitro helps elucidate these pathways.
Purpose of the Study:
- To investigate Plasmodium falciparum invasion pathways in Kenyan isolates.
- To determine if specific invasion profiles correlate with malaria severity.
- To compare invasion phenotypes between Kenyan and Gambian P. falciparum isolates.
Main Methods:
- Studied invasion pathways of 31 Kenyan P. falciparum isolates from children with malaria.
- Erythrocytes were treated with neuraminidase, trypsin, and chymotrypsin to identify invasion profiles.
- Compared invasion phenotypes between isolates from severe and uncomplicated malaria cases.
Main Results:
- Six distinct invasion profiles were identified among the 31 Kenyan isolates.
- The majority (23/31) exhibited neuraminidase-resistant, trypsin-sensitive invasion (receptor X pathway).
- Only 3/31 isolates showed the neuraminidase-sensitive, trypsin-sensitive phenotype (EBA-175/glycophorin A pathway).
- No significant association was found between invasion profiles and malaria severity.
- No difference in enzyme inhibition levels between severe and uncomplicated malaria isolates.
Conclusions:
- Invasion pathway differences do not appear to significantly influence Plasmodium falciparum malaria virulence.
- The dominant invasion pathway in Kenyan isolates differs from that in Gambian isolates.
- Significant knowledge gaps remain regarding the molecular basis of invasion in natural P. falciparum infections.
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