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DECREASE OF BOUND SIALIC ACID AND INHIBITOR IN CHORIOALLANTOIC MEMBRANES INFECTED WITH INFLUENZA VIRUS

机译:感染了流感病毒的短铝变质膜中有价唾液酸和抑制剂的降低

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摘要

Tess, Bernard R. (University of Illinois at the Medical Center, Chicago) and J. Emerson Kempf. Decrease of bound sialic acid and inhibitor in chorioallantoic membranes infected with influenza virus. J. Bacteriol. >86:239–245. 1963.—During the adsorption period after the inoculation of chick embryos with the PR8 strain of influenza A virus, bound sialic acid (BSiA) in the chorioallantoic membranes decreased, presumably as a result of cleavage of surface glycoprotein by the viral neuraminidase. A further decrease occurred between 1 and 6 hr after infection, indicating that cleavage of the surface glycoprotein was continuing, and that the enzyme may have begun to act upon intracellular glycoprotein. Decreased levels of BSiA continued until 48 hr after infection, possibly as a result of continued intracellular enzyme activity plus destruction of glycoprotein as virus was released from the surface of the cells. BSiA began to increase 48 hr after infection, presumably because of regeneration of glycoprotein and its decreased destruction by the viral enzyme, since the process of infection was largely completed. Heat-stable hemagglutination inhibitor did not begin to decrease until 8 hr after infection; thereafter, the levels of BSiA and inhibitor appeared to be related.
机译:Tess,Bernard R.(伊利诺伊大学芝加哥分校医学中心)和J. Emerson Kempf。感染流感病毒的绒毛尿囊膜中结合唾液酸和抑制剂的减少。 J.细菌。 > 86: 239-245。 1963年。在鸡胚接种甲型流感病毒PR8株后的吸附期间,绒毛膜尿囊膜中结合的唾液酸(BSiA)减少,可能是由于病毒神经氨酸酶切割了表面糖蛋白所致。感染后1至6小时之间进一步减少,表明表面糖蛋白的切割仍在继续,并且该酶可能已开始作用于细胞内糖蛋白。 BSiA水平的降低一直持续到感染后48小时,这可能是由于细胞内酶活性的不断增强以及糖蛋白的破坏所致,因为病毒从细胞表面释放出来。感染后48小时,BSiA开始增加,可能是由于糖蛋白的再生及其被病毒酶破坏的程度有所降低,因为感染过程已基本完成。直到感染后8小时,热稳定的血凝抑制剂才开始减少。此后,BSiA和抑制剂的水平似乎相关。

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