Kuhn E M, Mätz-Rensing K, Stahl-Hennig C, Makoschey B, Hunsmann G, Kaup F J
Working Group Experimental Pathology, German Primate Centre, Göttingen, Germany.
Zentralbl Veterinarmed B. 1997 Oct;44(8):501-12. doi: 10.1111/j.1439-0450.1997.tb01001.x.
Intestinal lesions were studied in 32 rhesus monkeys experimentally infected with different strains of simian immunodeficiency virus SIVmac (251/32H, 251/32H-SPL and 251/MPBL) by light microscopy, transmission and scanning electron microscopy. A spectrum of primary and secondary manifestations of SIV-infection were detected. Primary changes included 'SIV-enteropathy' in 12 monkeys and virus-induced syncytial giant cell formation (GCF) of the intestine in two animals. A primary virus-induced enteropathy occurred both as only histologically visible 'SIV-enteropathy' and as 'AIDS-enteropathy' accompanied by clinical signs of enteritis. Secondary opportunistic infections (Balantidium coli, Cryptosporidium, Trichuris, Trichomonas, Spironucleus, Mycobacteria and Cytomegalovirus) were identified in 27 animals and three monkeys developed malignant lymphomas involving the intestinal tract. Compared to intestinal lesions in HIV-infected patients, differences were found concerning the incidence of GCF and the range of opportunistic infections, with cryptosporidium, cytomegalovirus and mycobacteria occurring in both SIV-infected macaques and AIDS patients. The present observations revealed that SIV-infected rhesus monkeys provide an excellent model both for studies on the pathogenesis of HIV-enteropathy and opportunistic infections and for the development of therapies against cryptosporidial, cytomegalovirus and mycobacteria infection. Comparison of three SIV-strains revealed differences in primary and secondary lesions observed: SIVmac251/MPBL was correlated with severe primary SIV-induced pathologic changes and SIVmac251-SPL-infected animals showed a higher incidence of malignant lymphomas.
通过光学显微镜、透射电子显微镜和扫描电子显微镜，对32只经不同株系的猴免疫缺陷病毒SIVmac（251/32H、251/32H - SPL和251/MPBL）实验感染的恒河猴的肠道病变进行了研究。检测到了SIV感染的一系列原发性和继发性表现。原发性变化包括12只猴子出现“SIV肠病”，2只动物肠道出现病毒诱导的合胞体巨细胞形成（GCF）。原发性病毒诱导的肠病既表现为仅在组织学上可见的“SIV肠病”，也表现为伴有肠炎临床症状的“艾滋病肠病”。在27只动物中发现了继发性机会性感染（结肠小袋纤毛虫、隐孢子虫、鞭虫、滴虫、螺旋体、分枝杆菌和巨细胞病毒），3只猴子发生了累及肠道的恶性淋巴瘤。与HIV感染患者的肠道病变相比，在GCF的发生率和机会性感染范围方面存在差异，隐孢子虫、巨细胞病毒和分枝杆菌在SIV感染的猕猴和艾滋病患者中均有发生。目前的观察结果表明，SIV感染的恒河猴为研究HIV肠病和机会性感染的发病机制以及开发针对隐孢子虫、巨细胞病毒和分枝杆菌感染的治疗方法提供了一个极好的模型。对三种SIV株系的比较揭示了观察到的原发性和继发性病变的差异：SIVmac251/MPBL与严重的原发性SIV诱导的病理变化相关，而SIVmac251 - SPL感染的动物恶性淋巴瘤的发生率更高。
