Schultze B, Enjuanes L, Cavanagh D, Herrler G
Institut für Virologie, Philipps-Universität Marburg, Germany.
Adv Exp Med Biol. 1993;342:305-10. doi: 10.1007/978-1-4615-2996-5_47.
Porcine transmissible gastroenteritis virus (TGEV) was found to resemble avian infectious bronchitis virus (IBV) in its interaction with erythrocytes. Inactivation of the receptors on erythrocytes by neuraminidase treatment and restoration of receptors by reattaching N-acetylneuraminic acid (Neu5Ac) to cell surface components indicated that alpha 2,3-linked Neu5Ac serves as a receptor determinant for TGEV as has been reported recently for IBV. Similar to IBV, the haemagglutinating activity of TGEV is evident only after pretreatment of virus with neuraminidase indicating that inhibitors on the virion surface have to be inactivated in order to induce the HA-activity of these viruses. A model is presented to explain why the HA-activity of untreated virus is masked and how neuraminidase treatment results in the unmasking of this activity.
研究发现,猪传染性胃肠炎病毒(TGEV)在与红细胞的相互作用方面类似于禽传染性支气管炎病毒(IBV)。用神经氨酸酶处理使红细胞上的受体失活,并通过将N-乙酰神经氨酸(Neu5Ac)重新连接到细胞表面成分来恢复受体,这表明α2,3连接的Neu5Ac作为TGEV的受体决定簇,正如最近报道的IBV一样。与IBV相似,TGEV的血凝活性仅在病毒用神经氨酸酶预处理后才明显,这表明病毒粒子表面的抑制剂必须失活才能诱导这些病毒的血凝活性。本文提出了一个模型,以解释未处理病毒的血凝活性为何被掩盖,以及神经氨酸酶处理如何导致这种活性的暴露。