Relevant bibliographies by topics / Malaria susceptibility

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Malaria susceptibility'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Malaria susceptibility"

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Haldar, Kasturi, and Narla Mohandas. "Malaria, erythrocytic infection, and anemia." Hematology 2009, no. 1 (January 1, 2009): 87–93. http://dx.doi.org/10.1182/asheducation-2009.1.87.

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Abstract Malaria is a major world health problem. It results from infection of parasites belonging to the genus Plasmodium. Plasmodium falciparum and Plasmodium vivax cause the major human malarias, with P falciparum being the more virulent. During their blood stages of infection, both P falciparum and P vivax induce anemia. Severe malarial anemia caused by P falciparum is responsible for approximately a third of the deaths associated with disease. Malarial anemia appears to be multi-factorial. It involves increased removal of circulating erythrocytes as well as decreased production of erythrocytes in the bone marrow. The molecular mechanisms underlying malarial anemia are largely unknown. Over the last five years, malaria parasite ligands have been investigated for their remodeling of erythrocytes and possible roles in destruction of mature erythrocytes. Polymorphisms in cytokines have been associated with susceptibility to severe malarial anemia: these cytokines and malaria “toxins” likely function by perturbing erythropoiesis. Finally a number of co-infections increase susceptibility to malarial anemia, likely because they exacerbate inflammation caused by malaria. Because of the complexities involved, the study of severe malarial anemia may need a “systems approach” to yield comprehensive understanding of defects in both erythropoiesis and immunity associated with disease. New and emerging tools such as (i) mathematical modeling of the dynamics of host control of malarial infection, (ii) ex vivo perfusion of human spleen to measure both infected and uninfected erythrocyte retention, and (iii) in vitro development of erythroid progenitors to dissect responsiveness to cytokine imbalance or malaria toxins, may be especially useful to develop integrated mechanistic insights and therapies to control this major and fatal disease pathology.
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Scanlon, Seth Thomas. "Variable malaria susceptibility." Science 372, no. 6544 (May 20, 2021): 804.1–805. http://dx.doi.org/10.1126/science.372.6544.804-a.

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Burhan, Hira, Askari Syed Hasan, Syed Mansur-ul-Haque, Ghazanfar Zaidi, Taha Shaikh, and Aisha Zia. "Association between blood group and susceptibility to malaria and its effects on platelets, TLC, and Hb." Journal of Infection in Developing Countries 10, no. 10 (October 31, 2016): 1124–28. http://dx.doi.org/10.3855/jidc.6828.

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Introduction: According to the World Health Organization, the estimated number of malaria cases in Pakistan is about 1.5 million. Hematological variables like platelets, total leukocyte count (TLC), and hemoglobin (Hb) need to be evaluated to diagnose malaria in suspects. This study aimed to investigate the association between blood group and susceptibility to malaria and effects on platelets, TLC, and Hb. Methodology: This was a case-control study with a sample size of 446, of which 224 were malarial cases and 222 were controls. A designated questionnaire was developed to know age, gender, malarial strain, Hb, TLC, platelets, and blood group. Results: Of 224 malarial cases, 213 were P. vivax, and 11 were P. falciparum. There were 58 patients with blood group A, 72 with group B, 69 were O and 23 were AB. There was no significant difference in the blood group of controls compared to malarial patients (p > 0.05). Mean Hb level was 11.5mg/dL in malaria patients and 12.5mg/dL in controls. There was significant difference (p<0.01) in the mean platelet count in malarial (11,7000/μL) and control (24,5000/μL) patients. All blood groups showed similar falls in Hb and platelet levels, showing no significant difference among blood groups (p = 0.79 and p = 0.52, respectively). TLC was not significant between malarial and control groups (p = 0.072). Males were two times susceptible to malaria. Conclusions: There was no significant association between the type of blood group and susceptibility to malaria or developing anemia or thrombocytopenia.
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ICHIMORI, Kazuyo. "Mosquito susceptibility to malaria." Medical Entomology and Zoology 40, no. 1 (1989): 1–12. http://dx.doi.org/10.7601/mez.40.1_1.

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Jha, Aditya Nath, Pandarisamy Sundaravadivel, Vipin Kumar Singh, Sudhanshu S. Pati, Pradeep K. Patra, Peter G. Kremsner, Thirumalaisamy P. Velavan, Lalji Singh, and Kumarasamy Thangaraj. "MBL2Variations and Malaria Susceptibility in Indian Populations." Infection and Immunity 82, no. 1 (October 14, 2013): 52–61. http://dx.doi.org/10.1128/iai.01041-13.

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ABSTRACTHuman mannose-binding lectin (MBL) encoded by theMBL2gene is a pattern recognition protein and has been associated with many infectious diseases, including malaria. We sought to investigate the contribution of functionalMBL2gene variations toPlasmodium falciparummalaria in well-defined cases and in matched controls. We resequenced the 8.7 kb of the entireMBL2gene in 434 individuals clinically classified with malaria from regions of India where malaria is endemic. The study cohort included 176 patients with severe malaria, 101 patients with mild malaria, and 157 ethnically matched asymptomatic individuals. In addition, 830 individuals from 32 socially, linguistically, and geographically diverse endogamous populations of India were investigated for the distribution of functionalMBL2variants. TheMBL2 −221C(X) allelic variant is associated with increased risk of malaria (mild malaria odds ratio [OR] = 1.9, correctedPvalue [PCorr] = 0.0036; severe malaria OR = 1.6,PCorr= 0.02). The exon1 variantsMBL2*B(severe malaria OR = 2.1,PCorr= 0.036; mild versus severe malaria OR = 2.5,PCorr= 0.039) andMBL2*C(mild versus severe malaria OR = 5.4,PCorr= 0.045) increased the odds of having malaria. The exon1MBL2*D/*B/*Cvariant increased the risk for severe malaria (OR = 3.4,PCorr= 0.000045). The frequencies of low MBL haplotypes were significantly higher in severe malaria (14.2%) compared to mild malaria (7.9%) and asymptomatic (3.8%). TheMBL2*LYPAhaplotypes confer protection, whereasMBL2*LXPAincreases the malaria risk. Our findings in Indian populations demonstrate thatMBL2functional variants are strongly associated with malaria and infection severity.
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Baliyan, Vinit, Jeyaseelan Nadarajah, Atin Kumar, and Zohra Ahmad. "Cerebral malaria: susceptibility weighted MRI." Asian Pacific Journal of Tropical Disease 5, no. 3 (March 2015): 239–41. http://dx.doi.org/10.1016/s2222-1808(14)60661-7.

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Aitman, Timothy J., Lisa D. Cooper, Penny J. Norsworthy, Faisal N. Wahid, Jennefer K. Gray, Brian R. Curtis, Paul M. McKeigue, et al. "Malaria susceptibility and CD36 mutation." Nature 405, no. 6790 (June 2000): 1015–16. http://dx.doi.org/10.1038/35016636.

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Hernandez-Valladares, Maria, Pascal Rihet, and Fuad A. Iraqi. "Host susceptibility to malaria in human and mice: compatible approaches to identify potential resistant genes." Physiological Genomics 46, no. 1 (January 1, 2014): 1–16. http://dx.doi.org/10.1152/physiolgenomics.00044.2013.

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There is growing evidence for human genetic factors controlling the outcome of malaria infection, while molecular basis of this genetic control is still poorly understood. Case-control and family-based studies have been carried out to identify genes underlying host susceptibility to malarial infection. Parasitemia and mild malaria have been genetically linked to human chromosomes 5q31-q33 and 6p21.3, and several immune genes located within those regions have been associated with malaria-related phenotypes. Association and linkage studies of resistance to malaria are not easy to carry out in human populations, because of the difficulty in surveying a significant number of families. Murine models have proven to be an excellent genetic tool for studying host response to malaria; their use allowed mapping 14 resistance loci, eight of them controlling parasitic levels and six controlling cerebral malaria. Once quantitative trait loci or genes have been identified, the human ortholog may then be identified. Comparative mapping studies showed that a couple of human and mouse might share similar genetically controlled mechanisms of resistance. In this way, char8, which controls parasitemia, was mapped on chromosome 11; char8 corresponds to human chromosome 5q31-q33 and contains immune genes, such as Il3, Il4, Il5, Il12b, Il13, Irf1, and Csf2. Nevertheless, part of the genetic factors controlling malaria traits might differ in both hosts because of specific host-pathogen interactions. Finally, novel genetic tools including animal models were recently developed and will offer new opportunities for identifying genetic factors underlying host phenotypic response to malaria, which will help in better therapeutic strategies including vaccine and drug development.
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Kwiatkowski, D. "Genetic susceptibility to malaria getting complex." Current Opinion in Genetics & Development 10, no. 3 (June 1, 2000): 320–24. http://dx.doi.org/10.1016/s0959-437x(00)00087-3.

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Bonn, Dorothy. "Susceptibility to malaria during pregnancy explained." Lancet 352, no. 9138 (October 1998): 1447. http://dx.doi.org/10.1016/s0140-6736(05)61271-8.

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Dissertations / Theses on the topic "Malaria susceptibility"

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Cunnington, Aubrey Justin. "Malaria and susceptibility to other infections." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2012. http://researchonline.lshtm.ac.uk/901045/.

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Malaria is widely perceived as immunosuppressive. Despite extensive phenomenological description, the underlying mechanisms remain poorly described. The aim of this thesis was to identify possible mechanisms by which malaria modifies host defence, and to determine the importance of these mechanisms in a translational system moving from a mouse model to human malaria. The most frequently cited immunological consequences of malaria are: suppression of vaccine responses, susceptibility to bacterial infection, susceptibility to endemic Burkitt lymphoma, and increased HIV viral load. Of these, susceptibility to non-Typhoid Salmonella (NTS) bacteremia, associated with severe hemolysis, was the most consistent between animal and human studies. I hypothesized that hemolysis would induce the immunomodulatory enzyme heme oxygenase-l (HO-l), which is essential for survival in malaria infections in mice, but might impair host defence against NTS. I demonstrate in mice that malaria, chemically-induced hemolysis, or simply administration of heme, cause loss of resistance to NTS, allowing more rapid bacterial growth than in control animals. A new niche for bacterial replication is established within neutrophils, which have impaired oxidative burst and bacterial killing activity. Hemolysis and heme induce HO-1 in neutrophil progenitors in the bone marrow, and this reduces the oxidative burst capacity of maturing neutrophils whilst also causing their premature mobilization into the circulation. Inhibition of HO by the competitive inhibitor SnPP abrogates the impaired resistance to NTS infection. I observed a similar phenomenon in Gambian children with malaria, with prolonged impairment of neutrophil function, the severity of which is related to hemolysis and HO-l induction. In summary I have shown that hemolysis- and HO-l-mediated neutrophil dysfunction occurs in malaria and is important for susceptibility to NTS infection. HO-1 inhibition might offer a novel therapy to alleviate neutrophil dysfunction in malaria patients.
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Khor, Chiea Chuen. "Host genetic susceptibility to malaria and bacteraemia." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534216.

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Carpenter, Danielle. "Genetics of susceptibility to malaria and leishmaniasis." Thesis, University of Leeds, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396597.

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Sikora, Martin. "Evolutionary genetics of malaria: genetic susceptibility and natural selection." Doctoral thesis, Universitat Pompeu Fabra, 2010. http://hdl.handle.net/10803/7220.

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Una de les forces selectives més fortes que han afectat a les poblacions humanes en la història més recent és el paràsit de la malària: Plasmodium falciparum, que és la causa de varis exemples d'adaptació induïda per patògens en els éssers humans. Una forma especial de malària és l'associada a l'embaràs, que es caracteritza per l'acumulació d'eritròcits infectats en la placenta, i que pot arribar a causar fins a 200.000 morts maternoinfantils cada any. L'objectiu d'aquest treball és descriure com aquesta forma peculiar de malària ha afectat la variació genètica humana. Amb aquesta finalitat, hem utilitzat mètodes tant de la genètica evolutiva com de l'epidemiologia molecular, resultant en la primera investigació a gran escala de la base genètica de la malària placentària. Els resultats ofereixen una nova visió sobre els gens que modulen el risc d'infecció, ,així com de la selecció natural actuant sobre les vies cel·lulars implicades en la patogènesi de la malaltia. Finalment, també aportem noves dades sobre l'estructura genètica de les poblacions sub-saharianes analitzades.
One of the strongest selective forces affecting human populations in recent history is the malaria parasite Plasmodium falciparum, which is the cause of a variety of well-established examples of pathogen-induced adaptation in humans. A special form of malaria is pregnancy-associated malaria, which is characterised by the accumulation of infected erythrocytes in the placenta, and causes up to 200,000 maternal and infant deaths every year. The aim of this work is to characterise how this particular form of malaria has shaped human genetic variation. To that end we use methods of both evolutionary genetics and molecular epidemiology, reporting the first large-scale investigation of the genetic basis of placental infection. Our results provide new insights into genes modulating the risk of infection, as well as natural selection acting on cellular pathways involved in the pathogenesis of the disease. Finally, we also provide new data on the genetic structure of affected populations in Sub-Saharan Africa.
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Ruwende, Cyril. "Host genetic factors in susceptibility to malaria and tuberculosis." Thesis, University of Oxford, 1996. http://ora.ox.ac.uk/objects/uuid:2accb6c6-8a70-4320-8b8b-16e6e595b5ed.

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Plasmodium falciparum and Mycobacterium tuberculosis infections collectively cause as many as five million deaths world-wide each year. In the most afflicted populations, currently available drugs and vaccines appear inadequate. By offering insight into the pathophysiology of diseases, genetic studies provide options for new therapeutic approaches to major health problems. The results of case-control studies of genetic factors associated with disease outcomes in malaria and tuberculosis in an African setting are presented in this thesis. Glucose-6-Phosphate dehydrogenase (G6PD) deficiency, the commonest enzymopathy of humans, affects over 400 million people. The geographical correlation of its distribution with the historical endemicity of malaria suggests that this disorder has risen in frequency through natural selection by malaria. However, attempts to confirm that G6PD deficiency is protective in case-control studies of malaria have yielded conflicting results. Hence, for this X-linked disorder, it is unclear whether both male hemizygotes and female heterozygotes are protected or, as frequently suggested, only females. Furthermore, how much protection may be afforded is unknown. In two large case-control studies of over 2000 African children, I found that the common African form of G6PD deficiency (G6PD A-) is associated with a 46-58% reduction in risk of severe malaria for both female heterozygotes and male hemizygotes. A mathematical model incorporating the measured selective advantage against malaria suggests that a counterbalancing selective disadvantage, associated with this enzyme deficiency, has retarded its rise in frequency in malaria-endemic regions. There is some evidence that two T helper cell subsets, Thl and Th2, regulate the immune response and thus influence the course of infections in mammalian hosts. These T cell subsets are reciprocal and associated with distinct cytokine profiles. Th2 T cell differentiation is promoted mainly by interleukin-4. Analysis of an IL-4 promoter polymorphism indicates that homozygosity for a putatively upregulatory IL-4 promoter variant is associated with a signficantly increased risk for severe malaria whilst heterozygotes are protected against this condition. Epidemiological evidence implicates host genetic factors as major determinants of variable susceptibility to tuberculosis. Most attempts to define the genetic factor(s) have focused on the HLA genes but only one result, an association of HLA-DR2 with increased susceptibility to disease in Asian populations, has been reported with any consistency. The genetic component in tuberculosis is likely to be determined by multiple genes and, therefore, in this study, the role of both HLA and non-HLA candidate genes was investigated. No association was found with variants of the macrophage gene, NRAMP1, the homologue of which has been implicated in the regulation of genetic resistance in the mouse model. Examination of certain class I and class II HLA alleles as well as the -590 interleukin-4 promoter polymorphism also did not show any association with disease. However, heterozygotes for a promoter polymorphism at position -238 of the tumour necrosis factor gene and homozygotes for dysfunctional variants of the gene encoding the collectin, mannose binding protein, were both at increased risk of developing pulmonary tuberculosis.
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Sisay-Joof, Fatoumatta. "Immunogenetic studies on susceptibility of West Africans to malaria." Thesis, Open University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392869.

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Ling, Edmund Y. S. "'Host genetic susceptibility to tuberculosis and malaria in Africa'." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491193.

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Humans have been afflicted with tuberculosis (TB) and malaria since antiquity. Although largely eradicated from the developed nations of Europe and North America, these diseases have remained a constant threat in the developing world, especially Asia and Africa. TB a~d malaria are multifactorial infectious diseases which have been shown to have a strong genetic component, through twin studies, genome-wide linkage studies and candidate gene association studies. A partial genome screen, utilising microsatellite markers from chromosomes 2, 5, 6, 15, 19,20,21 and 22, ofTB in Algerian affected sibling pair families was undertaken for this thesis. The marker D5S641 on chromosome 5 located 'a region (5qI4.2) suggestive of linkage in TB (LOD 1.48, P=0.005). This thesis also reports research on candidate genes for TB and malaria' in West Africa. The incidence of TB in West African males is more than twice that of females. Nevertheless, no association was found between TB and the Y chromosome polymorphisms studied. Analysis of Y chromosome SNP markers confirmed that case and control groups were adequately matched in the West African' TB study. The Y chromosome data ·also showed that the paternal gene pool of these West African populations were distinct from those of their geographical and linguistic neighbours. Conversely, the evidence from mitochondrial DNA supported a proposed migration of females into the study region, resulting in a greater similarity of the maternal gene pools among populations in West Africa. ' This thesis focussed particularly on candidate genes involved in pathogen pattern recognition receptor pathways, and identified several such genes that appeared to be associated with TB. Heterozygotes for the TIRAP SNP, rs8177374, were found to be protected against TB (OR=4.38, 95% C.1. 1.37 to 13.96, Pcorrected=O.013), supporting parallel work implicating this variant in protection against other infectious diseases. A non-synonymous coding SNP, rs1990760, of IFIHI, a gene which encodes a cytoplasmic receptor for certain pathogen-associated molecular patterns, also provided evidence of association with TB, with heterozygotes for the SNP being more susceptible (OR=1.83, 95% C.I. 1.27 to 2.62, PcorrecterO.OOl). TT homozygotes for the non-synonymous coding SNP, rs1884444, of IL23R also showed greater susceptibility to TB than individuals with the alternate allele, G (OR=1.50, 95% C.1. 1.05 to 2.14, PcorrecterO.026). There was no evidence for association of TLR9, TICAM2, IRF3, IRF5, IRF7 and MCPI with TB, nor PKLR and BTLA with malaria. ' . These findings ·add to our understanding of the multigenie basis of variable resistance to these· diseases and provide further evidence for the importance of innate immunity genes in affecting susceptibility.
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Cockburn, Ian. "Complement receptor one polymorphisms and susceptibility to severe malaria." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/13435.

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Rosetting – the binding of parasitized red blood cells to uninfected red cells to form “rosettes” has been associated with severe disease in many studies in Africa. However, a study in Papua New Guinea found no association between resetting and severe disease. It remains unclear whether resetting is a cause or correlate of parasite virulence. Rosetting is mediated by the interaction of at least one parasite protein: Plasmodium falciparum erythrocyte membrane protein one (PfEMP1) on the infected erythrocyte surface and a variety of host red cell surface receptors including complement receptor one (CR1). We reasoned that if resetting were a cause of severe disease we would be able to identify protective polymorphisms in the CR1 gene. Here we show that CR1 deficiency is extremely common among individuals from malaria endemic populations in Papua New Guinea. This deficiency is associated with previously reported polymorphisms in the CR1 gene and unexpectedly with alpha-thalassaemia, a red cell disorder that occurs in up to 90% of Melanesians. We tested the hypothesis that CR1 polymorphisms protect against severe malaria by genotyping samples from a case control study for polymorphisms in the CR1. We found that both CR1 deficiency alleles and alpha-thalassaemia protect against severe malaria. We wished to test the hypothesis that resetting was not associated with severe disease in Papua New Guinea because of widespread CR1 deficiency preventing the formation of rosettes strong enough to withstand sheer forces in the circulation. Studies on field isolates from Papua New Guinea showed that resetting was unusual in this population, rarely mediated by binding to CR1 and not associated with disease severity. This suggests that CR1 is essential for physiologically significant resetting associated with severe malaria. We have therefore identified a new malaria resistance gene and provided compelling evidence that CR1 mediated resetting is an important virulence phenotype and a potential target for drug vaccine development.
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Kimathi, Peter Opiyo. "Leveraging genotypes imputation and polygenic risk scores in malaria susceptibility." Master's thesis, Faculty of Health Sciences, 2020. http://hdl.handle.net/11427/32271.

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Background Over the past few years, Genome Wide Association Studies (GWAS) have identified thousands of genetic variants that are associated with a wide range of complex traits, and have provided valuable insights as far as their genetic architectures are concerned. In malaria studies too, GWAS has been successful and a number of genetic variants have been identified. Despite the success, the complete aetiology of malaria, and many complex traits in general, remains poorly understood. A key concern is that the missing heritability remains too large, with some of the variants identified in some populations failing to replicate using independent study populations. Indeed comparable sources have revealed that the statistical power of association studies can be improved either via genotypes imputation approaches or by treating the whole genome of an individual as a risk predictor using Polygenic Risk Scores (PRS). However, imputation remains at modest in Africa populations with few (or no) studies (study) have evaluated the potential of imputation tools in African populations. On the other hand, although the utility of PRS has been shown in other studies, it has neither been assessed in African population nor applied in an infectious disease, like malaria. Methodology We evaluated the performance of five popular genotypes imputation methods (IMPUTE4, minimac 4, IMPUTE2, minimac3 and BEAGLE4) using case control datasets that mimics African populations, European populations and the admixed populations simulated with FractalSIM. We assessed imputation performance based on internal imputation quality metrics and the genotypes concordance. We applied the best imputation tool based on the assessment results to impute raw genotypes data of severe malaria case control studies from MalariaGEN of three African populations: Kenya, The Gambia and Malawi. Similarly, we obtained summary statistics of the same datasets, and imputed the summary statistics with ImpG. We performed an association on the imputed raw genotypes, and compared the association results with that of ImpG based imputation. Additionally, we performed meta-analysis with METASOFT, and compared the meta-analysis result of ImpG based imputation and that from imputed raw genotypes associations. Finally, we assessed five PRS methods (PRSice, LDpred(p+t), PRSoS, PLINK and PRScS) in predicting genetic risk in African population, and applied the best PRS method to predict the genetic risk of severe malaria. Results IMPUTE2 recorded the best performance based on imputation accuracy and concordance for the African (accuracy=80.21% and concordance=99.2%) and the admixed samples (accuracy=69.46% and concordance=90.92%) for variants with MAF>0.05. Other tools recorded similar accuracy and concordance although BEAGLE 4 recorded the lowest concordance and accuracy across all the African and admixed datasets. For the real genotypes data, no SNP attained the genome wide significant threshold of 5.0 × 10−8 for Malawi and the Gambia datasets. However, for the Kenyan dataset, 9 SNPs on chromosome 11 were significantly associated with severe malaria. 3 of these SNPS were located on the HBG2 genes and the remaining 6 had not been reviewed. No SNP attained the genome wide threshold for the ImpG imputed summary statistics for all the populations. For IMPUTE2 based meta-analysis, only one SNP rs12295158 located on the HBB region was significant across all the meta-analysis model (with P-value of 2.88 × 10−12 for fixed (FE), 2.88 × 10−12 random (RE) and 9.64 × 10−12 binary effect (BE) respectively). On the other hand ImpG based meta-analysis, two SNPs were signicant across all the meta-analysis model (rs183731078 located on RFX3 with P-values of 8.40 × 10−9 , 8.40 × 10−9 , 4.47 × 10−8 for FE, RE and BE respectively, and rs8096513 located on DLGAP1 1.43 × 10−9 , 1.43 × 10−9 , 1.01 × 10−8 with P-value for FE, RE and BE respectively). Pathway enrichment and analysis of these genes revealed that both of these genes are associated with malaria. Finally, for the PRS, PRSoS recorded the best performance based on Nargalkerke's R 2 (0.01736) and area under curve (AUC) (0.511). Other PRS methods recorded slightly similar results with PLINK recording the least. The odds of having severe malaria was estimated as 2.869, and a unit change of PRS scores was associated with -5.143 change in odds of having severe malaria with P-value of 0.0193 at α = 0.05. However, the scores could only explain 1.28% of the phenotypic variance. Conclusion Our results provide foundation for future studies in genetics, especially in African population, where the best performing imputation tool remains a mystery. Moreover, our results have demonstrated the potential of application of PRS in infectious diseases.
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Steiner, Kevin Lee. "Prenatal priming to malaria antigens increases susceptibility to HIV infection." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1321827400.

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Books on the topic "Malaria susceptibility"

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Malaria resistance or susceptibility in red cells disorders. Hauppauge, NY: Nova Science, 2009.

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1955-, Walker Cheryl, ed. Genetics and cancer susceptibility: Implications for risk assessment. New York: Wiley-Liss, 1996.

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International, Conference on Carcinogenesis and Risk Assessment (8th 1994 Austin Tex ). Genetics and cancer susceptibility: Implications for risk assessment : proceedings of the Eighth International Conference on Carcinogenesis and Risk Assessment, held in Austin, Texas, November 30-December 3, 1994. New York: Wiley-Liss, 1996.

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Karasek, Micha. Aging And Age-Related Diseases: The Basics. Nova Biomedical Books, 2006.

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Book chapters on the topic "Malaria susceptibility"

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Kwiatkowski, Dominic P., and Gaia Luoni. "Host Genetic Factors in Resistance and Susceptibility to Malaria." In Molecular Approaches to Malaria, 462–79. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817558.ch24.

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Rai, Praveen Kumar, and Mahendra Singh Nathawat. "A Study of Malaria Susceptibility Mapping Using Statistical Methods with GIS." In Geoinformatics in Health Facility Analysis, 139–76. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44624-0_6.

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Motsholapheko, M. R., and B. N. Ngwenya. "Access to Water Resources and Household Vulnerability to Malaria in the Okavango Delta, Botswana." In African Handbook of Climate Change Adaptation, 1227–46. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-45106-6_165.

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AbstractMalaria is a persistent health risk for most rural communities in tropical wetlands of developing countries, particularly in the advent of climate change. This chapter assesses household access to water resources, livelihood assets, and vulnerability to malaria in the Okavango Delta of north-western Botswana. Data were obtained from a cross-sectional survey of 355 households, key informant interviews, PRA-based focus group discussions (FDGs), interviews with experts in various related fields, PRA workshop participant interviews, and literature review. There was high access to natural capital, and most households engaged in nature-based livelihood activities. Access to resources determined type of livelihood activities that households engaged in. However, there was no association between household exposure and/or susceptibility, and type of livelihood activities pursued by households. Household vulnerability to malaria was higher in remote and rural locations than in urban neighborhoods. Malaria prevention and vulnerability aversion programs need to be coupled with improvements in housing and well-being in the Okavango Delta and similar wetlands.
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Roberts, David J., Tyler Harris, and Thomas Williams. "The influence of inherited traits on malaria infection." In Susceptibility to Infectious Diseases, 139–84. Cambridge University Press, 2003. http://dx.doi.org/10.1017/cbo9780511546235.006.

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Campino, Susana G., and Taane G. Clark. ". Genetic Contribution to Malaria Susceptibility and Resistance." In Genomics and Health in the Developing World, 123–40. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780195374759.003.0013.

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Hofstetter, Douglas, Andrea Austin, and Ryan Maves. "Febrile Illness." In Acute Care Casebook, edited by Leslie V. Simon, 341–45. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190865412.003.0069.

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Malaria is a potentially life-threatening infection caused by several protozoa in the Plasmodium genus. Malaria is transmitted through the bite of a female Anopheles mosquito, which serves as the definitive host and vector of the disease. Geographically, malaria is normally found in warm, tropical climates that can support the Anopheles mosquito year-round. In uncomplicated malaria, signs and symptoms are often nonspecific. Due to the ongoing hemolysis, patients classically present with fevers followed by a characteristic paroxysm of chills, high fevers, and malaise. The classic gold standard for the diagnosis of malaria is light microscopy of Giemsa-stained peripheral blood smears. Pharmacotherapy depends on the suspected Plasmodium species, the local patterns of drug susceptibility, and the clinical status of the patient. Chemoprophylaxis is recommended for all individuals traveling to regions with endemic malaria.
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Kumar Ghosh, Susanta, and Chaitali Ghosh. "New Challenges in Malaria Elimination." In Current Topics and Emerging Issues in Malaria Elimination. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96532.

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In recent years, efforts to eliminate malaria has gained a tremendous momentum, and many countries have achieved this goal — but it has faced many challenges. Recent COVID-19 pandemic has compounded the challenges due to cessation of many on-field operations. Accordingly, the World Health Organization (WHO) has advocated to all malaria-endemic countries to continue the malaria elimination operations following the renewed protocols. The recent reports of artemisinin resistance in Plasmodium falciparum followed by indication of chloroquine resistance in P. vivax, and reduced susceptibility of synthetic pyrethroids used in long lasting insecticide nets are some issues hindering the elimination efforts. Moreover, long distance night migration of vector mosquitoes in sub-Saharan Africa and invasion of Asian vector Anopheles stephensi in many countries including Africa and Southeast Asia have added to the problems. In addition, deletion of histidine rich protein 2 and 3 (Pfhrp2/3) genes in P. falciparum in many countries has opened new vistas to be addressed for point-of-care diagnosis of this parasite. It is needed to revisit the strategies adopted by those countries have made malaria elimination possible even in difficult situations. Strengthening surveillance and larval source management are the main strategies for successful elimination of malaria. New technologies like Aptamar, and artificial intelligence and machine learning would prove very useful in addressing many ongoing issues related to malaria elimination.
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Ko, Wen-Ya, Felicia Gomez, and Sarah A. Tishkoff. "Evolution of human erythrocyte-specific genes involved in malaria susceptibility." In Rapidly Evolving Genes and Genetic Systems, 223–34. Oxford University Press, 2012. http://dx.doi.org/10.1093/acprof:oso/9780199642274.003.0022.

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Christiane Bougouma, Edith, and Sodiomon Bienvenu Sirima. "Inherited Disorders of Hemoglobin and Plasmodium falciparum Malaria." In Human Blood Group Systems [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.93807.

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An estimated 300,000 babies are born each year with severe Inherited Disorders of Hemoglobin (IDH). Despite major advances in the understanding of the molecular pathology, control, and management of the IDH thousands of infants and children with these diseases are dying due to the accessibility to appropriate medical care. In addition, as malaria has been the principal cause of early mortality in several parts of the world for much of the last 5000 years, as a result, it is the strongest force for selective pressure on the human genome. That is why, in the world, there is an overlap of malaria endemicity and IDH. Over the past twenty years several studies have shown that IDH such us hemoglobin and/or red cell membrane abnormalities confer resistance to malaria reducing hence the mortality during the first years of life. This has led to the selection of populations with IDH in malaria-endemic areas. This may explain the overlap between these two pathologies. This chapter aims to present the relationship between IDH and malaria susceptibility, make an overview of the current state of knowledge and the burden of IDH, and highlight steps that require to be taken urgently to improve the situation.
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McNicholl, Janet M., Marie V. Downer, Michael Aidoo, Thomas Hodge, and Venkatachalam Udhayakumar. "Public health assessment of genetic susceptibility to infectious diseases: malaria, tuberculosis, and HIV." In Genetics and Public Health in the 21st Century, 173–202. Oxford University Press, 2000. http://dx.doi.org/10.1093/acprof:oso/9780195128307.003.0010.

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Conference papers on the topic "Malaria susceptibility"

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Hincapié, Doracelly, and Juan Ospina. "Optimal control in a model of malaria with differential susceptibility." In SPIE Sensing Technology + Applications, edited by Šárka O. Southern, Mark A. Mentzer, Isaac Rodriguez-Chavez, and Virginia E. Wotring. SPIE, 2014. http://dx.doi.org/10.1117/12.2049782.

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Ould Lemrabott, Mohamed Aly. "Species composition and insecticide susceptibility of malaria vectors in two regions in Mauritania." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.108996.

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Kalimuthu, Hemalatha, Wooi Nee Tan, Sin Liang Lim, and Mohammad Faizal Ahmad Fauzi. "Assessing frequency ratio method for landslide susceptibility mapping in Cameron Highlands, Malaysia." In 2015 IEEE Student Conference on Research and Development (SCOReD). IEEE, 2015. http://dx.doi.org/10.1109/scored.2015.7449440.

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Chen, Jane, Mitch Matoga, Cecilia Massa, Beatrice Ndalama, Edward Jere, Robert Krysiak, Tarsizio Chikaonda, Marcia Hobbs, Myron Cohen, and Irving Hoffman. "P692 Gentamicin susceptibility toneisseria gonorrhoeaein malawi after twenty-five years of sustained use." In Abstracts for the STI & HIV World Congress (Joint Meeting of the 23rd ISSTDR and 20th IUSTI), July 14–17, 2019, Vancouver, Canada. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/sextrans-2019-sti.758.

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Latif, Zulkiflee Abd, Siti Nur Afiqah Aman, and Biswajeet Pradhan. "Landslide susceptibility mapping using LiDAR derived factors and frequency ratio model: Ulu Klang area, Malaysia." In 2012 IEEE 8th International Colloquium on Signal Processing & its Applications (CSPA). IEEE, 2012. http://dx.doi.org/10.1109/cspa.2012.6194753.

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Matori, A. N., and A. Basith. "Evaluation of landslide causative factors towards efficient landslide susceptibility modelling in the Cameron Highlands, Malaysia." In DEBRIS FLOWS. Southampton, UK: WIT Press, 2012. http://dx.doi.org/10.2495/deb120181.

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Younis, Khansa Mohammed, Gires Usup, and Asmat Ahmad. "A prospective study on evaluation of pathogenesis, biofilm formation, antibiotic susceptibility of microbial community in urinary catheter." In THE 2015 UKM FST POSTGRADUATE COLLOQUIUM: Proceedings of the Universiti Kebangsaan Malaysia, Faculty of Science and Technology 2015 Postgraduate Colloquium. AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4931227.

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Nordin, M. Helmi, M. Wahidullah Moh Wahi, Amresh Sashidharan, Nurfuzaini A. Karim, and Alif Syahrizad Ramli. "Feasibility Study on Optimisation of Material Selection for High Temperature Sour Gas Producer." In International Petroleum Technology Conference. IPTC, 2021. http://dx.doi.org/10.2523/iptc-21380-ms.

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Abstract K field is a green field in East Malaysia with prolific gas reserves that is being developed with six high rate gas producing wells from high temperature (190 °C) carbonate reservoir. Tubular material feasibility study is one of the key subjects of scrutiny when it comes to completing wells in high temperature environment coupled with existence of significant level of H2S and CO2 contents. Material testing was conducted at the specified test environments (102 bar CO2 + 120ppm H2S) and load cases to assess susceptibility of Martensitic Stainless Steel to Stress Corrosion Cracking (SCC), corrosion rate and compatibility with completion brine. The aim was to optimize the material selection that is fit for purpose (lower completion and flow-wetted area of production casing) and reduce well cost up to USD 2.5 million. The base case of material selection for flow-wetted section is 17CR110 ksi, which meets the design requirements of these wells based on fit for purpose test conducted in the data base. Flow-wetted section in this case is production liner and flow-wetted section of production casing below production packer. Super 13CR -110 ksi and 15CR125 ksi material grades were considered for design optimization for this section of interest. Four Point Bend Method was used for SCC test sets while weight loss method for corrosion rate measurement. For brine compatibility test, calcium bromide (without additive) was used as test solution for 17CR 110 ksi, 15CR 125 ksi and Super 13CR -110 ksi with elevated temperature of 190 °C. Post-test assessment was conducted by visual examination by stereomicroscope to check for surface indication and dye-penetrant examination to determine any indication of cracks. It was observed that the Super 13CR -110 ksi and 15CR 125 ksi test specimens survived the test with no pitting observed. Meanwhile, test specimens were weighed to determine corrosion rates, resulted to Super 13CR -110 ksi sample having an average corrosion rate of 0.2195 mm/year. This translates to less than 30% weight loss throughout well production life and therefore accepted for open-hole production liner and production casing flow-wetted section. Key enabler in this design optimization effort is the understanding of the Stress Corrosion Cracking for martensitic stainless steel in high temperature sour environment where commonly, martensitic stainless steel (Super 13Cr / Modified Super 13Cr) working temperature is 165 °C. The test manages to extend the working temperature up to 190 °C.
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