Bendinelli M, Pistello M, Lombardi S, Poli A, Garzelli C, Matteucci D, Ceccherini-Nelli L, Malvaldi G, Tozzini F
Department of Biomedicine, University of Pisa, Italy.
Clin Microbiol Rev. 1995 Jan;8(1):87-112. doi: 10.1128/CMR.8.1.87.
The lentivirus feline immunodeficiency virus (FIV) is a widespread pathogen of the domestic cat that is mainly transmitted through bites, although other means of transmission are also possible. Its prevalence ranges from 1 to 10% in different cat populations throughout the world, thus representing a large reservoir of naturally infected animals. FIV resembles the human immunodeficiency virus (HIV) in many respects. Similarities include the structural features of the virion, the general organization and great variability of the genome, the life cycle in the infected host, and most importantly, the pathogenic potential. Infection is associated with laboratory signs of immunosuppression as well as with a large variety of superinfections, tumors, and neurological manifestations. Our understanding of FIV is steadily improving and is providing important clues to the pathogenesis of immunodeficiency-inducing lentiviruses. The cellular receptor for FIV is different from the feline equivalent of the human CD4 molecule used by HIV; nevertheless, the major hallmark of infection is a progressive loss of CD4+ T lymphocytes as in HIV infection. The mechanisms by which FIV escapes the host's immune responses are being actively investigated. FIV causes lysis of infected T cells and also appears to predispose these cells to apoptosis. Infection of macrophages and other cell types has also been documented. For reasons yet to be understood, antibody-mediated neutralization of fresh FIV isolates is very inefficient both in vitro and in vivo. Vaccination studies have provided some encouraging results, but the difficulties encountered appear to match those met in HIV vaccine development. FIV susceptibility to antiviral agents is similar to that of HIV, thus providing a valuable system for in vivo preclinical evaluation of therapies. It is concluded that in many respects FIV is an ideal model for AIDS studies.
慢病毒猫免疫缺陷病毒(FIV)是家猫中一种广泛传播的病原体,主要通过咬伤传播,不过也存在其他传播途径。在世界各地不同的猫群体中,其流行率在1%至10%之间,因此代表着大量自然感染动物的储存库。FIV在许多方面类似于人类免疫缺陷病毒(HIV)。相似之处包括病毒体的结构特征、基因组的总体结构和高度变异性、在受感染宿主中的生命周期,以及最重要的致病潜力。感染与免疫抑制的实验室指标以及多种重叠感染、肿瘤和神经学表现有关。我们对FIV的理解正在稳步提高,并为诱导免疫缺陷的慢病毒的发病机制提供重要线索。FIV的细胞受体不同于HIV所使用的人类CD4分子的猫等同物;然而,感染的主要标志是如HIV感染一样CD4 + T淋巴细胞的逐渐丧失。FIV逃避宿主免疫反应的机制正在积极研究中。FIV导致受感染T细胞的裂解,并且似乎还使这些细胞易发生凋亡。巨噬细胞和其他细胞类型的感染也有记录。由于尚未明确的原因,新鲜FIV分离株的抗体介导中和在体外和体内都非常低效。疫苗接种研究取得了一些令人鼓舞的结果,但遇到的困难似乎与HIV疫苗开发中遇到的困难相当。FIV对抗病毒药物的敏感性与HIV相似,因此为体内治疗的临床前评估提供了一个有价值的系统。结论是,在许多方面FIV是艾滋病研究的理想模型。