Novel Insights into Plasmodium vivax Therapeutic Failure: CYP2D6 Activity and Time of Exposure to Malaria Modulate the Risk of Recurrence
Ana Carolina Rios Silvino, Flora Satiko Kano, Marcelo Azevedo Costa, Cor Jésus Fernandes Fontes, Irene S. Soares, Cristiana Ferreira Alves de Brito, Luzia H. Carvalho, Taís Nóbrega de Sousa
Abstract
Plasmodium vivax relapse is one of the major causes of sustained global malaria transmission. Primaquine (PQ) is the only commercial drug available to prevent relapses, and its efficacy is dependent on metabolic activation by cytochrome P450 2D6 (CYP2D6). Impaired CYP2D6 function, caused by allelic polymorphisms, leads to the therapeutic failure of PQ as a radical cure for P. vivax malaria. Here, we hypothesized that the host immune response to malaria parasites modulates susceptibility to P. vivax recurrences in association with CYP2D6 activity.
Topics & Concepts
PrimaquineMalariaPlasmodium vivaxCYP2D6BiologyChloroquineImmune systemVivax malariaImmunologyPharmacologyPlasmodium falciparumMedicineCytochrome P450Internal medicineMetabolismMalaria Research and ControlDrug Transport and Resistance MechanismsDrug-Induced Hepatotoxicity and Protection