TESS B R, KEMPF J E
J Bacteriol. 1963 Aug;86(2):239-45. doi: 10.1128/jb.86.2.239-245.1963.
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.
苔丝，伯纳德·R.（芝加哥伊利诺伊大学医学中心）和J. 爱默生·肯普夫。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。《细菌学杂志》86:239 - 245。1963年。——在用甲型流感病毒PR8株接种鸡胚后的吸附期内，绒毛尿囊膜中的结合唾液酸（BSiA）减少，推测是由于病毒神经氨酸酶裂解表面糖蛋白所致。感染后1至6小时之间进一步减少，表明表面糖蛋白的裂解仍在继续，并且该酶可能已开始作用于细胞内糖蛋白。BSiA水平持续下降直至感染后48小时，这可能是由于细胞内酶活性持续存在以及随着病毒从细胞表面释放糖蛋白被破坏所致。感染后48小时BSiA开始增加，推测是由于糖蛋白再生及其被病毒酶破坏减少，因为感染过程已基本完成。热稳定血凝抑制剂直到感染后8小时才开始减少；此后，BSiA和抑制剂的水平似乎相关。
