Science advances · 2019
The ferroportin Q248H mutation protects from anemia, but not malaria or bacteremia.
Клиническое исследованиеСтатьяМногоцентровое исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Muriuki John Muthii, Mentzer Alexander J, Band Gavin, Gilchrist James J, Carstensen Tommy, Lule Swaib A, Goheen Morgan M, Joof Fatou, Kimita Wandia, Mogire Reagan, Cutland Clare L, Diarra Amidou, Rautanen Anna, Pomilla Cristina, Gurdasani Deepti, Rockett Kirk, Mturi Neema, Ndungu Francis M, Scott J Anthony G, Sirima Sodiomon B, Morovat Alireza, Prentice Andrew M, Madhi Shabir A, Webb Emily L, Elliott Alison M, Bejon Philip, Sandhu Manjinder S, Hill Adrian V S, Kwiatkowski Dominic P, Williams Thomas N, Cerami Carla, Atkinson Sarah H
Аннотация
Iron acquisition is critical for life. Ferroportin (FPN) exports iron from mature erythrocytes, and deletion of the Fpn gene results in hemolytic anemia and increased fatality in malaria-infected mice. The FPN Q248H mutation (glutamine to histidine at position 248) renders FPN partially resistant to hepcidin-induced degradation and was associated with protection from malaria in human studies of limited size. Using data from cohorts including over 18,000 African children, we show that the Q248H mutation is associated with modest protection against anemia, hemolysis, and iron deficiency, but we found little evidence of protection against severe malaria or bacteremia. We additionally observed no excess Plasmodium growth in Q248H erythrocytes ex vivo, nor evidence of selection driven by malaria exposure, suggesting that the Q248H mutation does not protect from malaria and is unlikely to deprive malaria parasites of iron essential for their growth.