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Parasite-host interaction in malaria: genetic clues and copy number variation

In humans, infections contribute highly to mortality and morbidity rates worldwide. Malaria tropica is one of the major infectious diseases globally and is caused by the protozoan parasite Plasmodium falciparum. Plasmodia have accompanied human beings since the emergence of humankind. Due to its pat...

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Detalles Bibliográficos
Autores principales: Faik, Imad, de Carvalho, Elisandra Grangeiro, Kun, Jürgen FJ
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768989/
https://www.ncbi.nlm.nih.gov/pubmed/19725943
http://dx.doi.org/10.1186/gm82
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author Faik, Imad
de Carvalho, Elisandra Grangeiro
Kun, Jürgen FJ
author_facet Faik, Imad
de Carvalho, Elisandra Grangeiro
Kun, Jürgen FJ
author_sort Faik, Imad
collection PubMed
description In humans, infections contribute highly to mortality and morbidity rates worldwide. Malaria tropica is one of the major infectious diseases globally and is caused by the protozoan parasite Plasmodium falciparum. Plasmodia have accompanied human beings since the emergence of humankind. Due to its pathogenicity, malaria is a powerful selective force on the human genome. Genetic epidemiology approaches such as family and twin studies, candidate gene studies, and disease-association studies have identified a number of genes that mediate relative protection against the severest forms of the disease. New molecular approaches, including genome-wide association studies, have recently been performed to expand our knowledge on the functional effect of human variation in malaria. For the future, a systematic determination of gene-dosage effects and expression profiles of protective genes might unveil the functional impact of structural alterations in these genes on either side of the host-parasite interaction.
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spelling pubmed-27689892010-09-02 Parasite-host interaction in malaria: genetic clues and copy number variation Faik, Imad de Carvalho, Elisandra Grangeiro Kun, Jürgen FJ Genome Med Review In humans, infections contribute highly to mortality and morbidity rates worldwide. Malaria tropica is one of the major infectious diseases globally and is caused by the protozoan parasite Plasmodium falciparum. Plasmodia have accompanied human beings since the emergence of humankind. Due to its pathogenicity, malaria is a powerful selective force on the human genome. Genetic epidemiology approaches such as family and twin studies, candidate gene studies, and disease-association studies have identified a number of genes that mediate relative protection against the severest forms of the disease. New molecular approaches, including genome-wide association studies, have recently been performed to expand our knowledge on the functional effect of human variation in malaria. For the future, a systematic determination of gene-dosage effects and expression profiles of protective genes might unveil the functional impact of structural alterations in these genes on either side of the host-parasite interaction. BioMed Central 2009-09-02 /pmc/articles/PMC2768989/ /pubmed/19725943 http://dx.doi.org/10.1186/gm82 Text en Copyright ©2009 BioMed Central Ltd
spellingShingle Review
Faik, Imad
de Carvalho, Elisandra Grangeiro
Kun, Jürgen FJ
Parasite-host interaction in malaria: genetic clues and copy number variation
title Parasite-host interaction in malaria: genetic clues and copy number variation
title_full Parasite-host interaction in malaria: genetic clues and copy number variation
title_fullStr Parasite-host interaction in malaria: genetic clues and copy number variation
title_full_unstemmed Parasite-host interaction in malaria: genetic clues and copy number variation
title_short Parasite-host interaction in malaria: genetic clues and copy number variation
title_sort parasite-host interaction in malaria: genetic clues and copy number variation
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768989/
https://www.ncbi.nlm.nih.gov/pubmed/19725943
http://dx.doi.org/10.1186/gm82
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