ArticlePloS one2010
Transforming growth factor beta 2 and heme oxygenase 1 genes are risk factors for the cerebral malaria syndrome in Angolan children.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 3 of them syntheses that pooled it.
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Who cites it
30 citing papers in PubMed, 3 syntheses or guidelines pooled it, 49 citations in OpenAlex.
- HMOX1 STR polymorphism and malaria: an analysis of a large clinical dataset.Malaria journal · 2022Pooled it
- Pooled it
- The Role of Heme Oxygenase-1 Promoter Polymorphisms in Perinatal Disease.International journal of environmental research and public health · 2021Pooled it
- Plasma advanced oxidative protein products are associated with anti-oxidative stress pathway genes and malaria in a longitudinal cohort.Malaria journal · 2014Trial
- Targeting circulating labile heme as a defense strategy against malaria.Life science alliance · 2024Article
- Identifying adaptive alleles in the human genome: from selection mapping to functional validation.Human genetics · 2021Review
- Variation in genes implicated in B-cell development and antibody production affects susceptibility to pemphigus.Immunology · 2021Article
- Haem oxygenase protects against thrombocytopaenia and malaria-associated lung injury.Malaria journal · 2020Article
- Genetics of Malaria Inflammatory Responses: A Pathogenesis Perspective.Frontiers in immunology · 2019Review
- The Effect of ABO Blood Groups, Hemoglobinopathy, and Heme Oxygenase-1 Polymorphisms on Malaria Susceptibility and Severity.The Korean journal of parasitology · 2018Article
- Heme oxygenase-1 genetic variants and the conundrum of hyperbilirubinemia in African-American newborns.Journal of perinatology : official journal of the California Perinatal Association · 2018Article
- Could Heme Oxygenase-1 Be a New Target for Therapeutic Intervention in Malaria-Associated Acute Lung Injury/Acute Respiratory Distress Syndrome?Frontiers in cellular and infection microbiology · 2018Review
- Evaluation of the relationship between MARCO and CD36 single-nucleotide polymorphisms and susceptibility to pulmonary tuberculosis in a Chinese Han population.BMC infectious diseases · 2017Article
- Repeat polymorphisms in the Homo sapiens heme oxygenase-1 gene in diabetic and idiopathic gastroparesis.PloS one · 2017Article
- Pathophysiological Mechanisms in Gaseous Therapies for Severe Malaria.Infection and immunity · 2016Review
- The Iron age of host-microbe interactions.EMBO reports · 2015Review
- Polymorphisms in the Haem Oxygenase-1 promoter are not associated with severity of Plasmodium falciparum malaria in Ghanaian children.Malaria journal · 2015Article
- Differential positive selection of malaria resistance genes in three indigenous populations of Peninsular Malaysia.Human genetics · 2015Article
- NOS2 variants reveal a dual genetic control of nitric oxide levels, susceptibility to Plasmodium infection, and cerebral malaria.Infection and immunity · 2014Article
- Modeling malaria infection and immunity against variant surface antigens in Príncipe Island, West Africa.PloS one · 2014Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCerebral malaria (CM) represents a severe outcome of the Plasmodium falciparum infection. Recent genetic studies have correlated human genes with severe malaria susceptibility, but there is little data on genetic variants that increase the risk of developing specific malaria clinical complications. Nevertheless, susceptibility to experimental CM in the mouse has been linked to host genes including Transforming Growth Factor Beta 2 (TGFB2) and Heme oxygenase-1 (HMOX1). Here, we tested whether those genes were governing the risk of progressing to CM in patients with severe malaria syndromes. METHODOLOGY/PRINCIPAL
findingsWe report that the clinical outcome of P. falciparum infection in a cohort of Angolan children (n = 430) correlated with nine TGFB2 SNPs that modify the risk of progression to CM as compared to other severe forms of malaria. This genetic effect was explained by two haplotypes harboring the CM-associated SNPs (Pcorrec. = 0.035 and 0.036). In addition, one HMOX1 haplotype composed of five CM-associated SNPs increased the risk of developing the CM syndrome (Pcorrec. = 0.002) and was under-transmitted to children with uncomplicated malaria (P = 0.036). Notably, the HMOX1-associated haplotype conferred increased HMOX1 mRNA expression in peripheral blood cells of CM patients (P = 0.012). CONCLUSIONS/SIGNIFICANCE: These results represent the first report on CM genetic risk factors in Angolan children and suggest the novel hypothesis that genetic variants of the TGFB2 and HMOX1 genes may contribute to confer a specific risk of developing the CM syndrome in patients with severe P. falciparum malaria. This work may provide motivation for future studies aiming to replicate our findings in larger populations and to confirm a role for these genes in determining the clinical course of malaria.
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