Hoover E A, Mullins J I, Quackenbush S L, Gasper P W
Department of Pathology, Colorado State University, Fort Collins 80523.
Blood. 1987 Dec;70(6):1880-92.
We describe the identification, experimental transmission, and pathogenesis of a naturally occurring powerfully immunosuppressive isolate of feline leukemia virus (designated here as FeLV-FAIDS) which induces fatal acquired immunodeficiency syndrome (AIDS) in 100% (25 of 25) of persistently viremic experimentally infected specific pathogen-free (SPF) cats after predictable survival periods ranging from less than 3 months (acute immunodeficiency syndrome) to greater than one year (chronic immunodeficiency syndrome), depending on the age of the cat at time of virus exposure. The pathogenesis of FeLV-FAIDS-induced feline immunodeficiency disease is characterized by: a prodromal period of largely asymptomatic viremia; progressive weight loss, lymphoid hyperplasia associated with viral replication in lymphoid follicles, lymphoid depletion associated with extinction of viral replication in lymphoid follicles, intractable diarrhea associated with necrosis of intestinal crypt epithelium, lymphopenia, suppressed lymphocyte blastogenesis, impaired cutaneous allograft rejection, hypogammaglobulinemia, and opportunistic infections such as bacterial respiratory disease and necrotizing stomatitis. The clinical onset of immunodeficiency syndrome correlates with the replication of a specific FeLV-FAIDS viral variant, detected principally as unintegrated viral DNA, in bone marrow, lymphoid tissues, and intestine. Two of seven cats with chronic immunodeficiency disease that survived greater than 1 year after inoculation developed lymphoma affecting the marrow, intestine, spleen, and mesenteric nodes. Experimentally induced feline immunodeficiency syndrome, therefore, is a rapid and consistent in vivo model for prospective studies of the viral genetic determinants, pathogenesis, prevention, and therapy of retrovirus-induced immunodeficiency disease.
我们描述了一种自然发生的具有强大免疫抑制作用的猫白血病病毒分离株（在此命名为FeLV-FAIDS）的鉴定、实验性传播及发病机制。该病毒可在实验性感染的无特定病原体（SPF）猫中，于可预测的存活期后，使100%（25只中的25只）持续病毒血症的猫患上致命的获得性免疫缺陷综合征（AIDS）。存活期从不到3个月（急性免疫缺陷综合征）到超过1年（慢性免疫缺陷综合征）不等，这取决于猫在接触病毒时的年龄。FeLV-FAIDS诱导的猫免疫缺陷疾病的发病机制具有以下特点：前驱期为基本无症状的病毒血症；进行性体重减轻、与淋巴滤泡中病毒复制相关的淋巴组织增生、与淋巴滤泡中病毒复制消失相关的淋巴细胞耗竭、与肠隐窝上皮坏死相关的顽固性腹泻、淋巴细胞减少、淋巴细胞母细胞生成受抑制、皮肤同种异体移植排斥受损、低丙种球蛋白血症以及诸如细菌性呼吸道疾病和坏死性口炎等机会性感染。免疫缺陷综合征的临床发病与一种特定的FeLV-FAIDS病毒变异体的复制相关，该变异体主要以未整合的病毒DNA形式在骨髓、淋巴组织和肠道中被检测到。在接种后存活超过1年的7只患有慢性免疫缺陷疾病的猫中，有2只发生了影响骨髓、肠道、脾脏和肠系膜淋巴结的淋巴瘤。因此，实验性诱导的猫免疫缺陷综合征是一种快速且一致的体内模型，可用于前瞻性研究逆转录病毒诱导的免疫缺陷疾病的病毒基因决定因素、发病机制、预防和治疗。
