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Widespread platelet activation is not a prominent feature in Plasmodium vivax malaria.

JoÃo Conrado Khouri Dos Santos 1 ; Stefanie Costa Pinto Lopes 2 ; Erich Vinicius De-Paula ; Marcus Vinícius Guimarães de Lacerda 3 ; Fabio Costa 4
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Introduction. Platelets are important mediators of innate immunity. Moreover, thrombocytopenia is the most common hematological alteration during malaria. Therefore, platelets have been extensively studied in the context of malaria. However, their role in malaria pathogenesis is still ill-defined, especially for P. vivax infection. In this study, we assessed systemic platelet activation during vivax malaria through direct and indirect ways. Material and Methods. This study was approved by FMT-HVD Ethics Committee under CAAE: 54234216.1.0000.0005. Blood from malaria patients and controls was collected in ACD (15%). Complete blood counts were performed within 15 minutes in a Sysmex KX21N counter. Platelets were stained for flow cytometry, with PAC-1 (FITC), anti-CD62P (PE) and anti-CD61 (PerCp-Cy5.5). Platelet activation-related markers (CD40L, CD62P, CXCL4 and CXCL7) were measured in poor platelet plasma with a multiplex-based assay (R&D Systems). Results. The percentage of positivity for platelet activation did not differ between patients and controls in flow cytometry. Moreover, plasma from patients with malaria failed to induce activation of control platelets. Levels of circulating markers were significantly different only for CD40L, while CD62P and CXCL4 showed a nonsignificant trend towards higher levels in patients.CXCL7 levels were below the detection level for most samples of both patients and controls. Conclusion. Using both direct and indirect measurements, we did not find convincing evidence for widespread platelet activation during vivax malaria, a result in line with previous studies with falciparum malaria. Of the platelet activation-associated markers, only CD40L was significantly elevated. While this finding might suggest some grade of platelet activation, widespread platelet activation in vivax malaria is not a prominent feature of pathogenesis, in contrast with other thrombocytopenic infections, like dengue fever.