Usanga E A, Luzzatto L
Nature. 1985;313(6005):793-5. doi: 10.1038/313793a0.
There is impressive evidence from geographical data, studies in the field and in vitro culture work that genetically determined deficiency of glucose 6-phosphate dehydrogenase (G6PD) confers relative protection against the human malaria parasite, Plasmodium falciparum. G6PD is encoded by an X-chromosome-linked gene, and protection phenomenon is manifested in heterozygous females who are genetic mosaics but, surprisingly, not in hemizygous males with complete deficiency. We have shown previously that the parasite, when passaged serially through G6PD-deficient red cells, undergoes adaptive changes that gradually improve its ability to multiply in these deficient cells. To explain the above paradox, we now show that this adaptive process is associated with, and may consist in, the induction of synthesis of a novel G6PD coded by Plasmodium falciparum.
来自地理数据、实地研究和体外培养工作的大量证据表明，葡萄糖6磷酸脱氢酶（G6PD）的基因决定缺陷赋予了对人类疟原虫恶性疟原虫的相对保护作用。G6PD由一个X染色体连锁基因编码，保护现象在作为基因嵌合体的杂合子女性中表现出来，但令人惊讶的是，在完全缺乏该酶的半合子男性中却没有表现。我们之前已经表明，当疟原虫在G6PD缺陷的红细胞中连续传代时，会发生适应性变化，从而逐渐提高其在这些缺陷细胞中增殖的能力。为了解释上述矛盾，我们现在表明，这一适应性过程与恶性疟原虫编码的一种新型G6PD的合成诱导有关，并且可能就在于此。
