Abstract
BackgroundIn a previous study, using a molecular approach, we reported the presence of P. vivax in Namibia. Here, we have extended our investigation to the Duffy antigen genetic profile of individuals of the same cohort with and without Plasmodium infections.MethodsParticipants with P. vivax (n = 3), P. falciparum (n = 23) mono-infections and co-infections of P. vivax/P. falciparum (n = 4), and P. falciparum/P. ovale (n = 3) were selected from seven regions. Participants with similar age but without any Plasmodium infections (n = 47) were also selected from all the regions. Duffy allelic profile was examined using standard PCR followed by sequencing of amplified products. Sequenced samples were also examined for the presence or absence of G125A mutation in codon 42, exon 2.ResultsAll individuals tested carried the − 67 T > C mutation. However, while all P. vivax infected participants carried the c.G125A mutation, 7/28 P. falciparum infected participants and 9/41 of uninfected participants did not have the c.G125A mutation. The exon 2 region surrounding codon 42, had a c.136G > A mutation that was present in all P. vivax infections. The odds ratio for lack of this mutation with P. vivax infections was (OR 0.015, 95% CI 0.001–0.176; p = 0.001).ConclusionWe conclude that P. vivax infections previously reported in Namibia, occurred in Duffy negative participants, carrying the G125A mutation in codon 42. The role of the additional mutation c.136 G > A in exon 2 in P. vivax infections, will require further investigations.
Highlights
In a previous study, using a molecular approach, we reported the presence of P. vivax in Namibia
The mutation on Fyb is commonly seen in sub-Saharan Africans, while the F ya mutation is common in Papua New Guineans [15, 16]
Other rare Duffy antigen receptor for chemokines (DARC) polymorphisms that have been reported are the c.265C > T mutation in the Duffy glycoprotein gene (FY)*B allele leading to the FY*X allele, which has a reduced expression of the gene by 90% [21], and the c.298G > A mutation resulting in a codon change from Ala100Thr [22], that reduces the expression of the Duffy antigen in erythrocytes
Summary
In a previous study, using a molecular approach, we reported the presence of P. vivax in Namibia. The null mutation on the Fyb allele was thought to be responsible for resistance of invasion of reticulocytes by P. vivax in subSaharan Africans [17]. There have been cumulative evidence using microscopy and/or molecular tools for the presence of P. vivax parasites in Duffy negative individuals in Sub-Saharan Africans [18, 19]. Since most of these studies were performed with subjects who had mostly no travel history to known endemic areas, this raises the question as to whether P. vivax is emerging, having adapted to invade reticulocytes independent of DARC. It is possible that P. vivax infection did always occur in Duffy negative individuals, but its diagnosis was overlooked
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