Luján L, Begara I, Collie D, Watt N J
Department of Veterinary Pathology, Royal (Dick) School of Veterinary Studies, University of Edinburgh, UK.
Vet Pathol. 1994 Nov;31(6):695-703. doi: 10.1177/030098589403100610.
The expression of gag (p15, p25) and env gene products in ovine lentivirus-infected cells was studied in 20 adult Texel ewes seropositive to maedi-visna virus and 10 seronegative matched controls. Bronchoalveolar lavage was performed to recover alveolar cell pools from which cytocentrifuge preparations were made. Single and double immunocytochemical techniques were applied to study viral replication and coexpression of viral markers with markers for macrophages, lymphocytes, and major histocompatibility complex (MHC) class II. Aveolar macrophages of eight of 20 infected sheep (40%) were positive for viral protein expression. The percentage of positive macrophages varied from < 1% to 12% of the total population of macrophages. Viral protein expression was not detected in lymphocytes or other cell types. A relationship between virus-replicating macrophages and differential expression of MHC class II molecules, upregulated in ovine lentivirus infection, could not be established. Pathology was evaluated in nine infected ewes. Animals with the highest levels of positive cells had moderate or severe lymphoid interstitial pneumonia. However, sheep with similar degrees of lesions had lower percentages of positive macrophages or were negative for viral protein detection. These results support the idea that a partial or even a complete loss in the restriction mechanism of maedi-visna virus in lungs can occur in some individuals.
在20只对梅迪-维斯纳病毒血清呈阳性的成年特克塞尔母羊和10只血清呈阴性的匹配对照中，研究了慢病毒感染细胞中gag（p15、p25）和env基因产物的表达。进行支气管肺泡灌洗以回收肺泡细胞池，从中制备细胞离心涂片。应用单免疫细胞化学和双免疫细胞化学技术研究病毒复制以及病毒标志物与巨噬细胞、淋巴细胞和主要组织相容性复合体（MHC）II类标志物的共表达。20只受感染绵羊中有8只（40%）的肺泡巨噬细胞病毒蛋白表达呈阳性。阳性巨噬细胞的百分比占巨噬细胞总数的<1%至12%。在淋巴细胞或其他细胞类型中未检测到病毒蛋白表达。无法确定病毒复制巨噬细胞与绵羊慢病毒感染中上调的MHC II类分子差异表达之间的关系。对9只受感染母羊的病理情况进行了评估。阳性细胞水平最高的动物患有中度或重度淋巴间质性肺炎。然而，病变程度相似的绵羊阳性巨噬细胞百分比更低或病毒蛋白检测呈阴性。这些结果支持这样一种观点，即某些个体肺部的梅迪-维斯纳病毒限制机制可能会部分甚至完全丧失。
