Plasmodium malariae structure and genetic diversity in sub-Saharan Africa determined from microsatellite variants and linked SNPs in orthologues of antimalarial resistance genes
Plasmodium malariae , a neglected human malaria parasite, contributes up to 10% of malaria infections in sub-Saharan Africa (sSA). Though P. malariae infection is considered clinically benign, it presents mostly as coinfections with the dominant P. falciparum . Completion of its reference genome has...
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Published in: | Scientific reports Vol. 12; no. 1; pp. 21881 - 12 |
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Main Authors: | , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
London
Nature Publishing Group UK
19-12-2022
Nature Portfolio |
Subjects: | |
Online Access: | Get full text |
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Summary: | Plasmodium malariae
, a neglected human malaria parasite, contributes up to 10% of malaria infections in sub-Saharan Africa (sSA). Though
P. malariae
infection is considered clinically benign, it presents mostly as coinfections with the dominant
P. falciparum
. Completion of its reference genome has paved the way to further understand its biology and interactions with the human host, including responses to antimalarial interventions. We characterized 75
P. malariae
isolates from seven endemic countries in sSA using highly divergent microsatellites. The
P. malariae
infections were highly diverse and five subpopulations from three ancestries (independent of origin of isolates) were determined. Sequences of 11 orthologous antimalarial resistance genes, identified low frequency single nucleotide polymorphisms (SNPs), strong linkage disequilibrium between loci that may be due to antimalarial drug selection. At least three sub-populations were detectable from a subset of denoised SNP data from mostly the mitochondrial cytochrome
b
coding region. This evidence of diversity and selection calls for including
P. malariae
in malaria genomic surveillance towards improved tools and strategies for malaria elimination. |
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ISSN: | 2045-2322 2045-2322 |
DOI: | 10.1038/s41598-022-26625-w |