Abstract
Background Plasmodium vivax can potentially lead to life-threatening episodes but the mechanisms underlying severe disease remain poorly defined. Cytoadhesion of infected erythrocytes may contribute to P. vivax sequestration and organ injury although its physiological impact is still unknown. Here, we aimed to describe clinically-relevant cytoadhesive phenotypes of P. vivax isolates.Methodology/Principal findingsRosetting and adhesion to CSA, CD36, ICAM1, placental and brain cryosections were determined in P. vivax peripheral isolates from 12 pregnant women, 24 non-pregnant women and 23 men from Manaus (Brazil). P. falciparum co-infection was excluded by PCR and P. vivax isolates were genotyped by assessing the size polymorphism of microsatellites ms2, ms20 and msp1F3 through capillary electrophoresis of PCR products. P. vivax monoinfection was confirmed by PCR in 59 isolates, with 50 (85%) of them being single-clone infections. One P. vivax haplotype was more frequently found among pregnant women (33%) than in non-pregnant women (0%) and men (4%; p = 0.010). Rosetting was observed in 64% of the isolates, adhesion to CSA in 15%, to ICAM1 in 12% and to placental cryosections in 9%, being similar among pregnant and non-pregnant groups. Intensity of rosetting was higher among anaemic individuals compared to non-anaemic (p = 0.010) and decreased with increasing haematocrit (p = 0.033) and haemoglobin levels (p = 0.015).Conclusions/Significance P. vivax peripheral isolates from pregnant women do not exhibit a prominent adhesion to CSA, although other parasite phenotypes still unknown may increase the propagation of certain P. vivax clones observed among pregnant hosts. Rosetting is a frequent cytoadhesive phenotype in P. vivax infections that may contribute to the development of anaemia.
Highlights
Plasmodium vivax is an important cause of morbidity outside Africa [1] that can induce severe complications, including cerebral malaria, acute respiratory distress and severe anaemia [2,3], and potentially lead to life-threatening episodes [4]
The mechanisms contributing to severe disease in P. vivax malaria remain largely unknown, scarce evidences suggests that to P. falciparum, P. vivax may adhere to host receptors on the vascular endothelium or on uninfected erythrocytes to form ‘rosettes’
The present study aimed to describe clinically relevant cytoadhesive phenotypes of P. vivax infected erythrocytes isolated from peripheral blood of pregnant and non-pregnant patients in the Brazilian Amazon
Summary
Plasmodium vivax is an important cause of morbidity outside Africa [1] that can induce severe complications, including cerebral malaria, acute respiratory distress and severe anaemia [2,3], and potentially lead to life-threatening episodes [4]. The mechanisms underlying severe disease in P. vivax malaria remain poorly defined [5]. Recent studies have suggested that cytoadhesion and sequestration of infected erythrocytes (IE), a key pathogenic process involved in severe P. falciparum malaria [6], may contribute to severe disease in P. vivax [9,10,11,12]. Plasmodium vivax can potentially lead to life-threatening episodes but the mechanisms underlying severe disease remain poorly defined. We aimed to describe clinically-relevant cytoadhesive phenotypes of P. vivax isolates
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