抗瘧藥物通常只對(duì)部分種類的瘧原蟲(chóng)有效,，這是瘧疾防治一直以來(lái)的難題。英國(guó)研究人員日前在破解這一難題方面取得進(jìn)展,，他們發(fā)現(xiàn)了一種對(duì)所有惡性瘧原蟲(chóng)都有效的治療途徑,。

英國(guó)桑格研究所等機(jī)構(gòu)研究人員在《自然》雜志網(wǎng)站上報(bào)告說(shuō)，他們發(fā)現(xiàn)瘧原蟲(chóng)在人體血液中入侵紅細(xì)胞的時(shí)候,，紅細(xì)胞上一種名為basigin的蛋白質(zhì)和瘧原蟲(chóng)表面一種名為PfRh5的蛋白質(zhì)之間的聯(lián)系是至關(guān)重要的，如果用藥物阻礙它們之間建立聯(lián)系,，就可以防止瘧原蟲(chóng)入侵紅細(xì)胞,，從而打斷瘧原蟲(chóng)傳播瘧疾的進(jìn)程。

這一發(fā)現(xiàn)的重要意義在于,，它對(duì)所有種類的惡性瘧原蟲(chóng)都有效,。據(jù)介紹，瘧原蟲(chóng)非常“狡詐”,，入侵紅細(xì)胞的途徑非常多樣而富于變化,，此前所發(fā)現(xiàn)的一些能防止瘧原蟲(chóng)入侵紅細(xì)胞的途徑都只對(duì)部分瘧原蟲(chóng)有效,，而在本次研究中，研究人員測(cè)試了所有種類的惡性瘧原蟲(chóng),，發(fā)現(xiàn)這個(gè)干預(yù)途徑對(duì)它們都有效,。

研究人員加文·賴特說(shuō)，這相當(dāng)于發(fā)現(xiàn)了瘧原蟲(chóng)的“阿喀琉斯之踵”,，完全改變了科研人員對(duì)瘧原蟲(chóng)入侵進(jìn)程的看法,。研究人員認(rèn)為可以在此基礎(chǔ)上開(kāi)發(fā)出更加有效的瘧疾防治手段。（生物谷 Bioon.com)

doi:10.1038/nature10606
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PMID:
Basigin is a receptor essential for erythrocyte invasion by Plasmodium falciparum

Cécile Crosnier, Leyla Y. Bustamante, S. Josefin Bartholdson, Amy K. Bei, Michel Theron, Makoto Uchikawa, Souleymane Mboup, Omar Ndir, Dominic P. Kwiatkowski, Manoj T. Duraisingh, Julian C. Rayner & Gavin J. Wright

Erythrocyte invasion by Plasmodium falciparum is central to the pathogenesis of malaria. Invasion requires a series of extracellular recognition events between erythrocyte receptors and ligands on the merozoite, the invasive form of the parasite. None of the few known receptor–ligand interactions involved1, 2, 3, 4 are required in all parasite strains, indicating that the parasite is able to access multiple redundant invasion pathways5. Here, we show that we have identified a receptor–ligand pair that is essential for erythrocyte invasion in all tested P. falciparum strains. By systematically screening a library of erythrocyte proteins, we have found that the Ok blood group antigen, basigin, is a receptor for PfRh5, a parasite ligand that is essential for blood stage growth6. Erythrocyte invasion was potently inhibited by soluble basigin or by basigin knockdown, and invasion could be completely blocked using low concentrations of anti-basigin antibodies; importantly, these effects were observed across all laboratory-adapted and field strains tested. Furthermore, Oka− erythrocytes, which express a basigin variant that has a weaker binding affinity for PfRh5, had reduced invasion efficiencies. Our discovery of a cross-strain dependency on a single extracellular receptor–ligand pair for erythrocyte invasion by P. falciparum provides a focus for new anti-malarial therapies