Lairmore M D, Butera S T, Callahan G N, DeMartini J C
Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Fort Collins, CO 80523.
J Immunol. 1988 Feb 1;140(3):779-85.
Ovine lentiviruses share genome sequence, structural features, and replicative mechanisms with HIV, the etiologic agent of AIDS. A lamb model of lentivirus-induced lymphoid interstitial pneumonia, comparable to lymphoid interstitial pneumonia associated with pediatric AIDS, was used to investigate production of leukocyte-soluble mediators. Lentivirus-infected lambs and adult sheep with severe lymphoid interstitial pneumonia had significantly elevated levels of spontaneous interferon (IFN) production from pulmonary leukocytes compared with ovine lentiviruses-infected animals with mild or no lesions of lymphoid interstitial pneumonia or non-infected controls. However, peripheral blood mononuclear cells from lentivirus-infected lambs did not spontaneously release significant amounts of IFN. IFN production by pulmonary lymph node lymphocytes was enhanced in the presence of lentivirus-infected alveolar macrophages. Animals with lentivirus-induced disease and spontaneous IFN production had enhanced virus replication within tissues. The ovine lentiviruses-induced IFN had a m.w. of between 25,000 and 35,000 and was resistant to freeze/thawing procedures. The IFN activity was sensitive to trypsin and stable to low pH and heat. IFN with similar physical and biochemical properties was produced when ovine lentiviruses was added to control leukocyte cultures. IL-2 and PGE2 production and responses to mitogen by pulmonary lymph node lymphocytes of lentivirus-diseased lambs were not statistically different from control animals. Increased local production of IFN in lentivirus-infected host tissues may serve to accelerate the entry of leukocytes into virus-induced lesions promoting cell-mediated tissue damage and also provide increased numbers of cells for virus replication.
绵羊慢病毒与艾滋病的病原体人类免疫缺陷病毒（HIV）在基因组序列、结构特征和复制机制方面具有相似性。利用一种慢病毒诱导的淋巴间质性肺炎羔羊模型（类似于与儿童艾滋病相关的淋巴间质性肺炎）来研究白细胞可溶性介质的产生。与患有轻度或无淋巴间质性肺炎病变的绵羊慢病毒感染动物或未感染对照相比，慢病毒感染的羔羊和患有严重淋巴间质性肺炎的成年绵羊肺白细胞自发产生干扰素（IFN）的水平显著升高。然而，慢病毒感染羔羊的外周血单核细胞不会自发释放大量IFN。在存在慢病毒感染的肺泡巨噬细胞的情况下，肺淋巴结淋巴细胞的IFN产生会增强。患有慢病毒诱导疾病且自发产生IFN的动物组织内病毒复制增强。绵羊慢病毒诱导产生的IFN分子量在25,000至35,000之间，且对冻融程序具有抗性。IFN活性对胰蛋白酶敏感，对低pH和热稳定。当将绵羊慢病毒添加到对照白细胞培养物中时，会产生具有相似物理和生化特性的IFN。慢病毒感染羔羊的肺淋巴结淋巴细胞的IL-2和PGE2产生以及对有丝分裂原的反应与对照动物相比无统计学差异。慢病毒感染宿主组织中局部IFN产生的增加可能有助于加速白细胞进入病毒诱导的病变，促进细胞介导的组织损伤，并且还为病毒复制提供更多细胞。
