Abstract
α+Thalassemia Antagonizes the Malaria-protective Effects of Sickle-Cell Trait
Highlights
While the mechanisms by which hemoglobinopathies confer malaria protection are debated (Taylor et al, 2013), with the notable exception of HbAS, they do not seem to protect by suppressing parasite densities
Using RBCs from individuals with HbAS, α+thalassemia, or both, they performed experiments that measure cytoadherence, rosetting, and PfEMP1 expression of four P. falciparum lines. While their reductionist approach of using few parasite strains is a minor limitation of this study, they made up for this by using a large panel of RBCs from hemoglobinopathic donors (10–20 of each genotype) (Opi et al, 2014). Their findings largely confirm earlier reports that HbAS and α+thalassemia are each associated with impaired cytoadherence, rosetting, and PfEMP1 expression (Cholera et al, 2008; Krause et al, 2012), with two exceptions
Α+thalassemia increased PfEMP1 expression without affecting rosetting; for another, α+thalassemia increased PfEMP1 expression but paradoxically decreased cytoadherence. These findings contrast with those of Krause et al (2012), who generally found that α+thalassemia reduced both PfEMP1 expression and cytoadherence (α+thalassemia increased the cytoadherence of some parasite isolates)
Summary
While the mechanisms by which hemoglobinopathies confer malaria protection are debated (Taylor et al, 2013), with the notable exception of HbAS, they do not seem to protect by suppressing parasite densities. If α+thalassemia antagonizes malaria-protective effects of HbAS in the field, it should antagonize cytoadherence-weakening effects of HbAS in the laboratory.
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