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      Multiplicity of Plasmodium falciparum infection in asymptomatic children in Senegal: relation to transmission, age and erythrocyte variants

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          Abstract

          Background

          Individuals living in malaria endemic areas generally harbour multiple parasite strains. Multiplicity of infection (MOI) can be an indicator of immune status. However, whether this is good or bad for the development of immunity to malaria, is still a matter of debate. This study aimed to examine the MOI in asymptomatic children between two and ten years of age and to relate it to erythrocyte variants, clinical attacks, transmission levels and other parasitological indexes.

          Methods

          Study took place in Niakhar area in Senegal, where malaria is mesoendemic and seasonal. Three hundred and seventy two asymptomatic children were included. Sickle-cell trait, G6PD deficiency (A- and Santamaria) and α +-thalassaemia (-α 3.7 type) were determined using PCR. Multiplicity of Plasmodium falciparum infection, i.e. number of concurrent clones, was defined by PCR-based genotyping of the merozoite surface protein-2 ( msp2), before and at the end of the malaria transmission season. The χ 2-test, ANOVA, multivariate linear regression and logistic regression statistical tests were used for data analysis.

          Results

          MOI was significantly higher at the end of transmission season. The majority of PCR positive subjects had multiple infections at both time points (64% before and 87% after the transmission season). MOI did not increase in α-thalassaemic and G6PD mutated children. The ABO system and HbAS did not affect MOI at any time points. No association between MOI and clinical attack was observed. MOI did not vary over age at any time points. There was a significant correlation between MOI and parasite density, as the higher parasite counts increases the probability of having multiple infections.

          Conclusion

          Taken together our data revealed that α-thalassaemia may have a role in protection against certain parasite strains. The protection against the increase in MOI after the transmission season conferred by G6PD deficiency is probably due to clearance of the malaria parasite at early stages of infection. The ABO system and HbAS are involved in the severity of the disease but do not affect asymptomatic infections. MOI was not age-dependent, in the range of two to ten years, but was correlated with parasite density. However some of these observations need to be confirmed including larger sample size with broader age range and using other msp2 genotyping method.

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          Most cited references38

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          Biased distribution of msp1 and msp2 allelic variants in Plasmodium falciparum populations in Thailand.

          Plasmodium falciparum isolates were obtained from Thai patients attending a malaria clinic on the Thai-Kampuchean border over 4 cross-sectional surveys carried out at 3-monthly intervals. The genetic structure of the parasite populations was determined by nested polymerase chain reaction (PCR) amplification of polymorphic regions of 3 P. falciparum antigen genes: msp1, msp2 and glurp. Although a high degree of diversity characterized these isolates, the overall population structure of the parasites associated with patent malaria infections was observed to remain relatively stable over time. The highest degree of polymorphism was observed with msp2, and the mean number of lines per infection (multiplicity of infection) calculated with this marker was higher than that obtained using msp1 or glurp alone, or combined. Infections with > or = 2 parasite lines were seen in 76% of the samples, and were proportionally more numerous at the start and end of the rainy season. Two interesting exceptions to the random distribution were observed and involved 2 allelic variants which in one case were found dissociated (msp1 MAD20-family) and in the other were associated (msp2 FC27-family). The epidemiological significance of these types of data is discussed.
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            Human red blood cell polymorphisms and malaria.

            Genetic factors are a major determinant of child survival in malaria endemic countries. Identifying which genes are involved and how they affect the malaria disease risk potentially offers a powerful mechanism through which to learn more about the host-parasite relationship. The past few years have seen significant progress towards achieving this goal for some of the best-known malaria resistance genes that determine the structure or function of red blood cells: Gerbich blood group antigen negativity; polymorphisms of the complement receptor genes (most notably CR1); Southeast Asian ovalocytosis; pyruvate kinase deficiency; haemoglobin E; the sickle cell trait; and alpha-thalassaemia are all examples. The challenge for the future must be to translate such advances into fresh approaches to the prevention and treatment of malaria.
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              Host age as a determinant of naturally acquired immunity to Plasmodium falciparum.

              J. Baird (1995)
              The usual course of infection by Plasmodium falciparum among adults who lack a history of exposure to endemic malaria is fulminant. The infection in adults living with hyper- to holoendemic malaria is chronic and benign. Naturally acquired immunity to falciparum malaria is the basis of this difference. Confusion surrounds an essential question regarding this process: What is its rate of onset? Opinions vary because of disagreement over the relationships between exposure to infection, antigenic polymorphism and naturally acquired immunity. In this review, Kevin Baird discusses these relationships against a backdrop of host age as a determinant of naturally acquired immunity to falciparum malaria.
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                Author and article information

                Journal
                Malar J
                Malaria Journal
                BioMed Central
                1475-2875
                2008
                23 January 2008
                : 7
                : 17
                Affiliations
                [1 ]Department of Immunology, Stockholm University, S-106 91 Stockholm, Sweden
                [2 ]University of Buea, Buea, Cameroon
                [3 ]Institut de Recherche pour le Développement (IRD), Unité de Recherche 010 "Santé de la mère et de l'enfant en milieu tropical", BP 1386, Dakar, Senegal
                [4 ]IRD, UR 010, 08 BP 841, Cotonou, Benin
                Article
                1475-2875-7-17
                10.1186/1475-2875-7-17
                2267475
                18215251
                30938da6-d4fa-4a65-a552-d92da2c43e1f
                Copyright © 2008 Vafa et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 28 September 2007
                : 23 January 2008
                Categories
                Research

                Infectious disease & Microbiology
                Infectious disease & Microbiology

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