Molecular basis of cholera blood-group dependence and implications for a world characterized by climate change
Abstract
Climate change has the potential to increase the threat of water-borne diseases, through rises in temperature and sea-level, and precipitation variability. Cholera poses a particular threat, and the need to develop better intervention tools is imminent. Cholera infections are particularly severe for blood group O individuals, who are less protected by the current vaccines. Here we derive a hypothesis as to the molecular origins of blood-group dependence of this disease, based on relevant epidemiological, clinical and molecular data, and give suggestions on how to plan prevention strategies, and develop novel and improved pharmaceuticals.
Abbreviations: CT, cholera toxin, CTB, cholera toxin B pentamer, ETEC, enterotoxigenic Escherichia coli, Fuc, l-fucose, Gal, d-galactose, GalNAc, 2′-N-acetyl galactosamine, Glc, d-glucose, GlcNAc, 2′-N-acetyl glucosamine, LT, heat-labile enterotoxin of human isloates, LTB, heat-labile enterotoxin B pentamer of human isolates, WHO, World Health Organization
Keywords: Blood-group antigen recognition, Cholera toxin, Climate change/global warming, Protein–carbohydrate interaction, Structural biology, Vaccine development
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PII: S0014-5793(10)00330-3
doi:10.1016/j.febslet.2010.03.050
© 2010 Federation of European Biochemical Societies
