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On the relation between malaria and G-6-PD deficiency: a reply

SIR, We appreciate the opportunity to respond to the communication of Bottini et al. (p. 363 of this issue), especially as we feel that the apparent differences between these authors and ourselves are semantic to some extent. We hope here to clarify our views on the relation between G-6-PD deficiency and malaria. Bottini et al. go to some pains to document the fact that G-6-PD-deficient haemolytic crises in hemizygous males were extremely serious events before modem medical treatment, and that the added stress of malaria could hardly have made the condition selectively advantageous. We agree. In our previous communication (Huheey and Martin, 1975) we drew an analogy between G-6-PD deficiency and sickle cell disease, with respect to resistance to malaria. Though all analogies may be pushed too far, we believe that ours is a useful one in understanding the selective forces at work on what, at first glance, may appear to be a strictly deleterious gene. To look for positive selection for the gene for G-6-PD deficiency in 407