Wiedbrauk D L, Hadlow W J, Ewalt L C, Lodmell D L
J Virol. 1986 Aug;59(2):514-7. doi: 10.1128/JVI.59.2.514-517.1986.
Studies were done to determine whether differences in interferon production are responsible for the resistance of pastel mink to Aleutian disease. The abilities of normal pastel and sapphire mink to produce interferon when inoculated with either Newcastle disease virus or a synthetic polyribonucleotide, poly (I):poly (C), were identical, even to the production of a novel, acid-labile interferon. The resistance of pastel mink to Aleutian disease did not correlate with interferon production, because neither sapphire nor pastel mink produced detectable amounts of interferon when infected with either the Pullman strain of Aleutian disease virus (ADV) or the highly virulent Utah I strain. Sapphire mink infected with the Pullman strain responded normally to poly (I):poly (C) early in the course of the disease, but interferon production was impaired late, when the mink were hypergammaglobulinemic and had renal, vascular, and hepatic lesions. These data suggest that ADV Pullman neither stimulates nor interferes with interferon production in infected mink and may represent a mechanism whereby ADV can more readily establish infection.
开展了多项研究,以确定干扰素产生的差异是否是导致浅色水貂对阿留申病具有抗性的原因。正常浅色水貂和蓝宝石色水貂在接种新城疫病毒或合成多聚核糖核苷酸聚(I):聚(C)时产生干扰素的能力是相同的,甚至在产生一种新型的、酸不稳定干扰素方面也是如此。浅色水貂对阿留申病的抗性与干扰素产生无关,因为当用阿留申病病毒(ADV)的普尔曼毒株或高毒力的犹他I毒株感染时,蓝宝石色水貂和浅色水貂均未产生可检测量的干扰素。感染普尔曼毒株的蓝宝石色水貂在疾病早期对聚(I):聚(C)反应正常,但在水貂出现高γ球蛋白血症并伴有肾脏、血管和肝脏病变的后期,干扰素产生受到损害。这些数据表明,ADV普尔曼毒株既不刺激也不干扰受感染水貂体内干扰素的产生,这可能代表了ADV能够更轻易地建立感染的一种机制。