Pathogenesis of experimentally induced feline immunodeficiency virus infection in cats.
Pathogenesis of experimentally induced feline immunodeficiency virus infection in cats.
复制标题
DOI：
--
复制
发表时间：
1988-08
影响因子：
1
通讯作者：
J. Yamamoto;E. Sparger;E. Ho;P. Andersen;T. O'connor;C. P. Mandell;L. Lowenstine;R. Munn;N. Pedersen
中科院分区：
文献类型：
--
作者：
J. Yamamoto;E. Sparger;E. Ho;P. Andersen;T. O'connor;C. P. Mandell;L. Lowenstine;R. Munn;N. Pedersen
猫免疫缺陷病毒（FIV；以前称为猫T淋巴细胞亲嗜性慢病毒）是一种典型的慢病毒，在形态特征、蛋白质结构和逆转录酶方面与人免疫缺陷病毒和猴免疫缺陷病毒相似。然而，它在抗原性上不同。该病毒亲嗜原代和永久性猫T淋巴母细胞以及克兰德尔猫肾细胞。在测试的其他永久性猫非淋巴母细胞，以及人、狗、小鼠和绵羊的淋巴样和非淋巴样细胞中，该病毒均未生长。在对猫进行的短期接种研究中，自然中发现的猫免疫缺陷样综合征未通过实验诱导出来，但观察到了一个明显的感染初期阶段。接种后4至5周观察到发热和中性粒细胞减少；发热持续数天，中性粒细胞减少持续1至9周。同时出现持续2至9个月的全身性淋巴结病。接种后2周出现针对FIV的抗体，然后达到稳定水平。在接种后4至5周内从所有感染猫的血液中重新分离出病毒，并且在体液抗体反应存在的情况下病毒无限期持续存在。从血液、血浆、脑脊液和唾液中可回收病毒，但从初乳或乳汁中未回收。在一个自然感染猫群中，接触传播缓慢发生，但在实验感染的猫和易感的无特定病原体的猫一起饲养长达4至14个月的情况下未发生传播。然而，通过血液、血浆或感染性细胞培养液的胃肠外接种，感染很容易传播。在自然感染或实验感染的母猫所产的小猫中未观察到宫内和经乳传播。在FIV感染初期观察到的淋巴结病归因于淋巴样增生和滤泡发育不良。在1只实验诱导感染的猫中观察到骨髓增殖性疾病。
Feline immunodeficiency virus (FIV; formerly, feline T-lymphotropic lentivirus) is a typical lentivirus resembling human and simian immunodeficiency viruses in morphologic features, protein structure, and reverse transcriptase enzyme. It is antigenically dissimilar, however. The virus is tropic for primary and permanent feline T-lymphoblastoid cells and Crandell feline kidney cells. The virus did not grow in other permanent feline non-lymphoblastoid cells that were tested, or in lymphoid and non-lymphoid cells from man, dogs, mice, and sheep. During short-term inoculation studies in cats, the feline immunodeficiency-like syndrome found in nature was not experimentally induced, but a distinct primary phase of infection was observed. Fever and neutropenia were observed 4 to 5 weeks after inoculation; fever lasted several days, and neutropenia persisted from 1 to 9 weeks. Generalized lymphadenopathy that persisted for 2 to 9 months appeared at the same time. Antibodies to FIV appeared 2 weeks after inoculation and then plateaued. Virus was reisolated from the blood of all infected cats within 4 to 5 weeks after inoculation and persisted indefinitely in the face of humoral antibody response. Virus was recovered from blood, plasma, CSF and saliva, but not from colostrum or milk. Contact transmission was achieved slowly in one colony of naturally infected cats, but not between experimentally infected and susceptible specific-pathogen-free cats kept together for periods as long as 4 to 14 months. The infection was transmitted readily, however, by parenteral inoculation with blood, plasma, or infective cell culture fluids. In utero and lactogenic transmission were not observed in kittens born to naturally or experimentally infected queens. Lymphadenopathy observed during the initial stage of FIV infection was ascribed to lymphoid hyperplasia and follicular dysplasia. A myeloproliferative disorder was observed in 1 cat with experimentally induced infection.