Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616-5270, USA.
Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman, WA 99163, USA.
Viruses. 2018 May 24;10(6):280. doi: 10.3390/v10060280.
Our laboratory has serially reported on the virologic and immunopathologic features of a cohort of experimental feline immunodeficiency virus (FIV)-infected cats for more than eight years. At 8.09 years post infection (PI), one of these animals entered the terminal stage of infection, characterized by undulating hyperthermia, progressive anorexia, weight loss, and pancytopenia; the animal was not responsive to therapeutic interventions, necessitating euthanasia six weeks later (8.20 years PI). Subsequent analyses indicated that neoplastic lymphocytes infiltrated multiple cervical lymph nodes and a band-like region of the mucosal lamina propria within a segment of the intestine. Immunohistochemistry and T cell clonality testing determined that the nodal and intestinal lesions were independently arising from CD3 T cell lymphomas. In-situ RNA hybridization studies indicated that diffuse neoplastic lymphocytes from the cervical lymph node contained abundant viral nucleic acid, while viral nucleic acid was not detectable in lymphocytes from the intestinal lymphoma lesion. The proviral long terminal repeat (LTR) was amplified and sequenced from multiple anatomic sites, and a common clone containing a single nucleotide polymorphism was determined to be defective in response to phorbol myristate acetate (PMA)-mediated promoter activation in a reporter gene assay. This assay revealed a previously unidentified PMA response element within the FIV U3 region 3' to the TATA box. The possible implications of these results on FIV-lymphoma pathogenesis are discussed.
我们的实验室已经连续报道了一组实验性猫免疫缺陷病毒(FIV)感染猫的病毒学和免疫病理学特征超过八年。在感染后 8.09 年,其中一只动物进入了感染的终末期,表现为波动热、进行性厌食、体重减轻和全血细胞减少;该动物对治疗干预无反应,六周后(感染后 8.20 年)需要安乐死。随后的分析表明,肿瘤性淋巴细胞浸润了多个颈部淋巴结和肠黏膜固有层的带状区域。免疫组织化学和 T 细胞克隆性检测确定,淋巴结和肠病变分别来自 CD3 T 细胞淋巴瘤。原位 RNA 杂交研究表明,来自颈部淋巴结的弥漫性肿瘤性淋巴细胞含有丰富的病毒核酸,而来自肠淋巴瘤病变的淋巴细胞中则无法检测到病毒核酸。从多个解剖部位扩增并测序了前病毒长末端重复序列(LTR),并确定在报告基因测定中,一种含有单核苷酸多态性的常见克隆对佛波醇肉豆蔻酸酯(PMA)介导的启动子激活反应缺陷。该检测揭示了在 TATA 盒 3'端的 FIV U3 区域内一个以前未识别的 PMA 反应元件。这些结果对 FIV-淋巴瘤发病机制的可能影响将进行讨论。