Putkonen P, Kaaya E E, Böttiger D, Li S L, Nilsson C, Biberfeld P, Biberfeld G
Department of Immunology, Karolinska Institute, Stockholm, Sweden.
AIDS. 1992 Mar;6(3):257-63. doi: 10.1097/00002030-199203000-00002.
To study the pathogenicity of simian immunodeficiency virus (SIVsm) in cynomolgus monkeys in order to establish an animal model for human AIDS.
Thirty-three cynomolgus monkeys were monitored for more than 2 years following experimental infection with SIVsm.
All the macaques became SIV-infected, as demonstrated by virus recovery from peripheral blood lymphocytes and by the appearance of viral antibodies. SIVsm was found to be pathogenic, killing 29 out of the 33 monkeys (88%) within 26 months. Clinically, infected monkeys developed lymphadenopathy, splenomegaly, diarrhoea, weight loss, neurological symptoms and a remarkably high incidence (39%) of malignant lymphomas. All lymphomas were high-grade malignant and of B-cell origin. Disease progression was associated with low CD4+ lymphocyte count, involution of initially hyperplastic follicular B-cell areas in lymph nodes, reappearance of viral antigen in serum, loss of anti-Gag antibodies and development of systemic giant cell disease in 55% of the monkeys.
There are many similarities between SIVsm-induced AIDS in cynomolgus monkeys and human AIDS with regard to clinical, virological, immunological and pathological manifestations.
研究猴免疫缺陷病毒（SIVsm）对食蟹猴的致病性，以建立人类艾滋病动物模型。
33只食蟹猴经SIVsm实验感染后，进行了2年多的监测。
所有猕猴均感染了SIV，这可通过从外周血淋巴细胞中分离出病毒以及出现病毒抗体得以证明。发现SIVsm具有致病性，在26个月内致使33只猴子中的29只（88%）死亡。临床上，受感染的猴子出现淋巴结病、脾肿大、腹泻、体重减轻、神经症状以及恶性淋巴瘤的高发病率（39%）。所有淋巴瘤均为高级别恶性且起源于B细胞。疾病进展与CD4 +淋巴细胞计数低、淋巴结中最初增生的滤泡性B细胞区域退化、血清中病毒抗原再次出现、抗Gag抗体丧失以及55%的猴子出现系统性巨细胞疾病有关。
SIVsm感染食蟹猴所致的艾滋病与人类艾滋病在临床、病毒学、免疫学和病理学表现方面有许多相似之处。
