Charley B, Laude H
Station de Virologie et d'Immunologie, Institut National de la Recherche Agronomique, Thiverval-Grignon, France.
J Virol. 1988 Jan;62(1):8-11. doi: 10.1128/JVI.62.1.8-11.1988.
Epithelial cells infected with the coronavirus transmissible gastroenteritis virus (TGEV) and fixed by glutaraldehyde induced a high alpha interferon (IFN-alpha) production in nonimmune porcine as well as human or bovine peripheral blood mononuclear cells (PBMC). IFN-alpha was detected as early as 3 h after exposure of PBMC to infected cells and at producer/inducer cell ratios as low as 1/1. Two of four monoclonal antibodies directed against the viral transmembrane glycoprotein E1 could block the IFN-inducing capacity of both TGEV-infected cells and viral particles. On the other hand, IFN-alpha induction was not markedly affected by monoclonal antibodies directed against other E1 epitopes, against peplomer glycoprotein E2, or against nucleocapsid protein. Thus, these findings strongly imply that IFN induction by TGEV results from interactions between an outer membrane domain of E1 and the PBMC membrane.
感染了冠状病毒性传染性胃肠炎病毒（TGEV）并用戊二醛固定的上皮细胞，在非免疫猪以及人或牛的外周血单核细胞（PBMC）中诱导产生了高浓度的α干扰素（IFN-α）。早在PBMC暴露于感染细胞后3小时，以及在生产者/诱导细胞比例低至1/1时，就检测到了IFN-α。四种针对病毒跨膜糖蛋白E1的单克隆抗体中有两种能够阻断TGEV感染细胞和病毒颗粒的IFN诱导能力。另一方面，针对其他E1表位、纤突糖蛋白E2或核衣壳蛋白的单克隆抗体对IFN-α的诱导没有明显影响。因此，这些发现强烈表明，TGEV诱导的IFN是由E1的外膜结构域与PBMC膜之间的相互作用产生的。
