2019
DOI: 10.1016/j.parint.2019.03.013
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Duffy antigen receptor for chemokines (DARC) and susceptibility to Plasmodium vivax malaria

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Cited by 5 publications
(5 citation statements)
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“…This hypothesis relies heavily on the existence of pathogens that are able to hijack chemokine receptors and use them to enter the cell. Some examples of such pathogens have indeed been identified, such as HIV-1, dengue virus (DENV), Epstein-Barr virus (EBV), and Plasmodium vivax [4][5][6][7][8][9][10][11]. Although DENV and EBV interactions with chemokine receptors remain somewhat elusive, it is well established that both HIV-1 and Plasmodium vivax interact directly with chemokine receptors in order to infect the cell [4,5,7,10,11].…”
Section: Resultsmentioning
confidence: 99%
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“…This hypothesis relies heavily on the existence of pathogens that are able to hijack chemokine receptors and use them to enter the cell. Some examples of such pathogens have indeed been identified, such as HIV-1, dengue virus (DENV), Epstein-Barr virus (EBV), and Plasmodium vivax [4][5][6][7][8][9][10][11]. Although DENV and EBV interactions with chemokine receptors remain somewhat elusive, it is well established that both HIV-1 and Plasmodium vivax interact directly with chemokine receptors in order to infect the cell [4,5,7,10,11].…”
Section: Resultsmentioning
confidence: 99%
“…Some examples of such pathogens have indeed been identified, such as HIV-1, dengue virus (DENV), Epstein-Barr virus (EBV), and Plasmodium vivax [4][5][6][7][8][9][10][11]. Although DENV and EBV interactions with chemokine receptors remain somewhat elusive, it is well established that both HIV-1 and Plasmodium vivax interact directly with chemokine receptors in order to infect the cell [4,5,7,10,11]. Site-directed mutagenesis has shown that HIV infection mainly depends on residues located in extracellular domains of CCR5, such as ECL1-3 and the N-terminus [11,13].…”
Section: Resultsmentioning
confidence: 99%
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“…Such differences may be highly significant, as the contributions of non-leukocytic cell types to protection against infection may be subject to evolutionary imprints from natural pathogens in both species that are at least as strong as those imposed on the innate immunity mediated by professional leukocytes. Classic examples include mutations of the human FUT2 gene conferring protection against intestinal norovirus infections (111); mutations of DARC and G6PD that prevent Plasmodium vivax infection in erythrocytes or reduce replication of this microbe in these cells (112); the sickle cell trait (heterozygosity for the HbS variant), which confers relative resistance to severe forms of P. falciparum malaria (54); and several other genetically encoded malaria-resistance traits phenotypically expressed by erythrocytes or erythrocyte precursors (113)(114)(115). Thus, despite the close relationship between the genomes of humans and mice, significant divergence exists, particularly within clusters of genes associated with immunity to infections.…”
Section: The Mouse and Human Genomes Differ At Immunological Locimentioning
confidence: 99%
“…The Duffy glycoprotein, a non-selective receptor, interacts with various chemokines such as interleukin-8 (IL-8) and melanoma growth-stimulating activity (MGSA) in the CXC group, as well as monocyte chemotactic protein-1 (MCP-1) and CCL5 in the CC group [5]. These interactions attract monocytes, memory CD4+ T lymphocytes, and eosinophils.…”
Section: Introductionmentioning
confidence: 99%