PATHOGENESIS OF ALEUTIAN DISEASE VIRUS INFECTION

这个项目的范围是阐明涉及到的致病机制 水貂感染阿留申水貂病细小病毒(ADV) 在过去的一年里，我们对感染adv的成年水貂进行了详细的研究。 采用免疫组织化学和链特异性原位杂交技术。 用抗血清进行免疫组织化学。 病毒粒子或ADV的非结构蛋白。对现场的修改 杂交程序将灵敏度提高了10到100倍， 但由于ADV在成年水貂中复制的限制性， 免疫组织化学和原位杂交相结合的方法 有可能。 10日龄成年水貂肠系膜淋巴结的免疫组织化学染色 在感染ADV-Utah 1后，ADV病毒粒子抗原在两个 2种细胞的胞核和胞浆。其中一个的形态是 巨噬细胞主要分布在延髓和其他类型 类似于抗原提呈的滤泡树突状细胞(FDC)在 生发中心。原位杂交揭示了复制的证据 (mRNA和复制形式DNA)在具有相同分布的细胞中， 然而，其他巨噬细胞和FDC似乎含有病毒DNA， 但不包括复制中间体(mRNA和复制形式DNA)。到60d 然而，在感染后，只在巨噬细胞中发现了活跃的复制。 这些结果表明，细胞与吞噬和抗原有关 演示文稿是整个过程中ADV复制的目标 感染。 此外，还观察到在感染60d后，AdV的复制 也发生在肾小管细胞和肾小球中，并且 复制与肾小球病理及肾脏脱屑的关系 肾小管细胞。这些研究表明，除了简单的机制外， 免疫复合体沉积可能参与了ADV肾脏的发生 疾病。

The scope of this project is to elucidate pathogenic mechanisms involved in infections of mink with Aleutian mink disease parvovirus (ADV). In the past year we performed detailed studies on ADV infected adult mink using immunohistochemistry and strand specific in situ hybridization. lmmunohistochemistry was performed using antiserum specific for either virion or nonstructural proteins of ADV. Modifications to the in situ hybridization procedure increased the sensitivity between 10 and 100-fold, but due to the restricted nature of ADV replication in adult mink, combination immunohistochemistry and in situ hybridization was not possible. Immunohistochemical staining of mesenteric lymph node from adult mink 10 d after infection with ADV-Utah 1 localized ADV virion antigen in both the nuclei and cytoplasm of 2 types of cells. One had the morphology of macrophages located primarily along medullary cords and the other type resembled antigen presenting follicular dendritic cells (FDC) found within germinal centers. In situ hybridization revealed evidence of replication (mRNA and replicative form DNA) in cells having an identical distribution, however, it appeared that other macrophages and FDC contained virion DNA, but not replicative intermediates (mRNA and replicative form DNA). By 60 d after infection, however, active replication was noted only in macrophages. These results suggested that cells involved with phagocytosis and antigen presentation were targets for ADV replication throughout the course of infection. In addition, it was observed that 60 d after infection ADV replication was also occurring in renal tubular cells and glomeruli and that the replication correlated with glomerular pathology and desquamation of renal tubular cells. These studies suggested that mechanisms other than simple immune complex deposition may be involved in the genesis of the ADV renal disease.