ADAPTATION OF PLASMODIUM-FALCIPARUM TO GLUCOSE-6-PHOSPHATE DEHYDROGENASE-DEFICIENT HOST RED-CELLS BY PRODUCTION OF PARASITE-ENCODED ENZYME
ADAPTATION OF PLASMODIUM-FALCIPARUM TO GLUCOSE-6-PHOSPHATE DEHYDROGENASE-DEFICIENT HOST RED-CELLS BY PRODUCTION OF PARASITE-ENCODED ENZYME
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DOI：
10.1038/313793a0
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发表时间：
1985-01-01
期刊：
影响因子：
64.8
通讯作者：
LUZZATTO, L
中科院分区：
文献类型：
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作者：
USANGA, EA;LUZZATTO, L
令人印象深刻的证据来自地理数据1,2，实地研究3和体外培养工作4 - 6，基因决定的葡萄糖6-磷酸脱氢酶（G6PD）缺乏赋予相对的保护对人类疟疾寄生虫，恶性疟原虫。G6PD由一个x染色体连接基因编码，这种保护现象在基因嵌合体的杂合子雌性中表现出来，但令人惊讶的是，在完全缺乏G6PD的半合子雄性中却没有表现出来。我们之前已经证明，当寄生虫连续通过缺乏g6pd的红细胞时，会经历适应性变化，逐渐提高其在这些缺乏g6pd的细胞中的繁殖能力。为了解释上述悖论，我们现在表明，这种适应过程与恶性疟原虫编码的新型G6PD的合成有关，并且可能存在于诱导合成中。
There is impressive evidence from geographical data1,2, studies in the field3andin vitroculture work4–6that 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 gene7, and protection phenomenon is manifested in heterozygous females who are genetic mosaics but, surprisingly, not in hemizygous males with complete deficiency8. 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 cells9. 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 byPlasmodium falciparum.