奥地利科学家日前发现了黄病毒入侵健康细胞的机理，从而为相关传染病的防治研究开辟了新途径。
黄病毒是一种微小包膜病毒，许多传染病病毒如登革热病毒、西尼罗河病毒、流行性乙脑病毒和初夏脑膜炎病毒等都属于黄病毒科。
奥地利维也纳医科大学病毒医学院的科学家发现，黄病毒可以使自己的细胞膜与被感染细胞的细胞膜融合，通过这种被称为“受体内吞”的机制，它将自身的遗传信息植入被感染细胞的细胞质中，从而入侵健康的肌体细胞。
科学家还在研究中发现，一种被称为“融合蛋白”的物质在黄病毒与宿主细胞融合过程中起着关键作用。这种蛋白对宿主细胞质的酸碱程度非常敏感，宿主细胞质的酸性程度越高越有利于黄病毒的入侵。
这一研究成果刊登在最新一期的美国《细胞生物学》杂志上。（生物谷Bioon.com）
生物谷推荐原始出处：
The Journal of Cell Biology, Vol. 183, No. 2, 353-361 doi:10.1083/jcb.200806081
Identification of specific histidines as pH sensors in flavivirus membrane fusion
Richard Fritz, Karin Stiasny, and Franz X. Heinz
Institute of Virology, Medical University of Vienna, 1095 Vienna, Austria
The flavivirus membrane fusion machinery, like that of many other enveloped viruses, is triggered by the acidic pH in endosomes after virus uptake by receptor-mediated endocytosis. It has been hypothesized that conserved histidines in the class II fusion protein E of these viruses function as molecular switches and, by their protonation, control the fusion process. Using the mutational analysis of recombinant subviral particles of tick-borne encephalitis virus, we provide direct experimental evidence that the initiation of fusion is crucially dependent on the protonation of one of the conserved histidines (His323) at the interface between domains I and III of E, leading to the dissolution of domain interactions and to the exposure of the fusion peptide. Conserved histidines located outside this critical interface were found to be completely dispensable for triggering fusion.
