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Differences between studies include varied study designs, sample sizes, inclusion of other known genetic modifiers (ie. sickle cell), and differences in the malaria phenotype being assessed.
For each malaria phenotype, we first performed statistical analyses of the data using multivariate regression analysis to take into account non-genetic factors such as age, year of study and transmission intensity (see Materials and Methods).
Patients were with different malaria phenotype were included: 276 mild, 37 Asymptomatic and 35 severe.
The largest study conducted to analyze ICAM-1Kilifi investigated more than 4,000 individuals, and no association with any malaria phenotype was observed [ 16].
The 1264G allele could provide a modest degree of protection from severe malaria (e.g. an OR between 0.95 and 1); protect from an infrequent but life-threatening malaria phenotype; or only offer protection to the rare deficiency allele homozygotes.
Alternatively, one or more co-insults may be necessary for development of the cerebral malaria phenotype, as malarial retinopathy is also seen in children with severe malarial anaemia without coma, albeit much less severely (Beare et al., 2004).
Similar(54)
Two categories of malaria phenotypes were considered in the study.
We tested the common haplotypes (frequency higher than 5%) within each LD block for association with severe malaria phenotypes.
We show here that both clinical and asymptomatic malaria phenotypes were under genetic control in these populations.
This study design enabled us to replicate the extent of genetic influence on malaria phenotypes identified in one village with the other.
We found that the different clinical malaria phenotypes can be discriminate according to their profile of IgG reactivity to brain antigens.
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