Paul Sondo; Biebo Bihoun; Bérenger Kabore; Marc Christian Tahita; Karim Derra; Toussaint Rouamba; Seydou Nakanabo Diallo; Adama Kazienga; Hamidou Ilboudo; Innocent Valea; Zekiba Tarnagda; Hermann Sorgho; Thierry Lefevre; Halidou Tinto
In: Pan Afr. Med. J., 39 , pp. 118, 2021, ISSN: 1937-8688, (Copyright: Paul Sondo et al. PMID: 34512854 PMCID: PMC8396377).
(Tags: Antimalarials/pharmacology, Burkina Faso, Drug Resistance, Falciparum/drug therapy/parasitology, GeneticRestriction Fragment Length, Genotype, Humans, Malaria, Membrane Transport Proteins/genetics, msp1, msp2, Multidrug Resistance-Associated Proteins/genetics, Mutation, Pfcrt, Pfmdr1, Plasmodium falciparum, Plasmodium falciparum/drug effects/genetics/isolation & purification, Polymerase Chain Reaction, Polymorphism, Protozoan Proteins/genetics)| | | |
Introduction: from a genetic point of view P. falciparumis
extremely polymorphic. There is a variety of parasite strains
infesting individuals living in malaria endemic areas. The
purpose of this study is to investigate the relationship between
polymorphisms in Plasmodium falciparum parasites and Pfcrt and
Pfmdr1 gene mutations in Nanoro area, Burkina Faso. Methods:
blood samples from plasmodium carriers residing in the Nanoro
Health District were genotyped using nested PCR. Parasite gene
mutations associated with resistance to antimalarial drugs were
detected by PCR-RFLP. Results: samples of 672 patients were
successfully genotyped. No msp1and msp2allelic families
exhibited an increase in developing mutations in resistance
genes. However, mutant strains of these genes were present at
greater levels in monoclonal infections than in multi-clonal
infections. Conclusion: this study provides an overview of the
relationship between polymorphisms in Plasmodium falciparum
parasites and mutations in resistance genes. These data will
undoubtedly contribute to improving knowledge of the parasite´s
biology and its mechanisms of resistance to antimalarial drugs.
Hamatandi Magloire Natama; Eduard Rovira-Vallbona; Meryam Krit; Pieter Guetens; Hermann Sorgho; M Athanase Somé; Maminata Traoré-Coulibaly; Innocent Valéa; Petra F Mens; Henk D F H Schallig; Dirk Berkvens; Luc Kestens; Halidou Tinto; Anna Rosanas-Urgell
In: Malar. J., 20 (1), pp. 94, 2021, ISSN: 1475-2875, (PMID: 33593344 PMCID: PMC7885350).
(Tags: Burkina Faso, Case-Control Studies, Cytokines, Falciparum/parasitology, Female, Genetic Predisposition to Disease/genetics, Humans, Immunity, Immunogenetic variants, Infant, Innate immunity, Innate/genetics, Malaria, Male, Plasmodium falciparum, Plasmodium falciparum/physiology)| | | |
BACKGROUND: Genetic polymorphisms in the human immune system
modulate susceptibility to malaria. However, there is a paucity
of data on the contribution of immunogenetic variants to malaria
susceptibility in infants, who present differential biological
features related to the immaturity of their adaptive immune
system, the protective effect of maternal antibodies and fetal
haemoglobin. This study investigated the association between
genetic variation in innate immune response genes and malaria
susceptibility during the first year of life in 656 infants from
a birth cohort survey performed in Nanoro, Burkina Faso.
METHODS: Seventeen single nucleotide polymorphisms (SNPs) in 11
genes of the immune system previously associated with different
malaria phenotypes were genotyped using TaqMan allelic
hybridization assays in a Fluidigm platform. Plasmodium
falciparum infection and clinical disease were documented by
active and passive case detection. Case-control association
analyses for both alleles and genotypes were carried out using
univariate and multivariate logistic regression. For cytokines
showing significant SNP associations in multivariate analyses,
cord blood supernatant concentrations were measured by
quantitative suspension array technology (Luminex). RESULTS:
Genetic variants in IL-1$beta$ (rs1143634) and
Fc$gamma$RIIA/CD32 (rs1801274)-both in allelic, dominant and
co-dominant models-were significantly associated with protection
from both P. falciparum infection and clinical malaria.
Furthermore, heterozygote individuals with rs1801274 SNP in
Fc$gamma$RIIA/CD32 showed higher IL-1RA levels compared to wild-type homozygotes (P = 0.024), a cytokine whose production
is promoted by the binding of IgG immune complexes to Fc$gamma$
receptors on effector immune cells. CONCLUSIONS: These findings
indicate that genetic polymorphisms in genes driving innate
immune responses are associated to malaria susceptibility during
the first year of life, possibly by modulating production of
Adama Gansané; Leah F Moriarty; Didier Ménard; Isidore Yerbanga; Esperance Ouedraogo; Paul Sondo; Rene Kinda; Casimir Tarama; Edwige Soulama; Madou Tapsoba; David Kangoye; Cheick Said Compaore; Ousmane Badolo; Blami Dao; Samuel Tchwenko; Halidou Tinto; Innocent Valea
In: Malar. J., 20 (1), pp. 48, 2021, ISSN: 1475-2875.
(Tags: Antimalarial, Antimalarials/pharmacology, Artemether, Artemether-lumefantrine, Artemisinins/pharmacology, Burkina Faso, Child, Dihydroartemisinin-piperaquine, Drug Resistance, Efficacy, Falciparum/drug therapy, Female, Lumefantrine Drug Combination/pharmacology, Malaria, Male, Plasmodium falciparum, Preschool, Quinolines/pharmacology)| | | |
BACKGROUND: The World Health Organization recommends regularly
assessing the efficacy of artemisinin-based combination therapy
(ACT), which is a critical tool in the fight against malaria.
This study evaluated the efficacy of two artemisinin-based
combinations recommended to treat uncomplicated Plasmodium
falciparum malaria in Burkina Faso in three sites: Niangoloko,
Nanoro, and Gourcy. METHODS: This was a two-arm randomized
control trial of the efficacy of artemether-lumefantrine (AL)
and dihydroartemisinin-piperaquine (DP). Children aged 6-59
months old were monitored for 42 days. The primary outcomes of
the study were uncorrected and PCR-corrected efficacies to day
28 for AL and 42 for DP. Molecular markers of resistance to
artemisinin derivatives and partner drugs were also analysed.
RESULTS: Of 720 children enrolled, 672 reached study endpoints
at day 28, 333 in the AL arm and 339 in the DP arm.
PCR-corrected 28-day per protocol efficacy in the AL arm was
74% (64-83%) in Nanoro, 76% (66-83%) in Gourcy, and 92%
(84-96%) in Niangoloko. The PCR-corrected 42-day per protocol
efficacy in the DP arm was 84% (75-89%) in Gourcy, 89%
(81-94%) in Nanoro, and 97% (92-99%) in Niangoloko. No Pfk13
mutation previously associated with artemisinin-resistance was
observed. No statistically significant association was found
between treatment outcome and presence of the 86Y mutation in
the Pfmdr1 gene. There was also no association observed between
treatment outcome and Pfpm2 or Pfmdr1 copy number variation.
CONCLUSION: The results of this study indicate evidence of
inadequate efficacy of AL at day 28 and DP at day 42 in the same
two sites. A change of first-line ACT may be warranted in
Burkina Faso. Trial Registry Pan African Clinical Trial Registry
Identifier: PACTR201708002499311. Date of registration: 8/3/2017
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