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环磷酰胺处理的恒河猴登革2型病毒感染研究

Studies on dengue 2 virus infection in cyclophosphamide-treated rhesus monkeys.

作者信息

Marchette N J, O'Rourke T, Halstead S B

出版信息

Med Microbiol Immunol. 1980 Feb;168(1):35-47. doi: 10.1007/BF02121650.

DOI:10.1007/BF02121650
PMID:6770237
Abstract

Dengue 2 virus (D2V) replication has been demonstrated in cultured primate mononuclear phagocytes, mitogen treated lymphocytes and lymphoblastoid cells. To determine which of these cell types might play an important role in sustaining infection in vivo, nine rhesus monkeys were immunosuppressed with cyclophosphamide and then infected with D2V. Maintenance dose which held total white blood cell counts to less than 3000/mm3 ablated both primary and secondary antibody responses. Six successfully immunosuppressed animals circulated virus and infected monocytes in blood for prolonged periods. Virus was recovered from lymphatic organs and visualized in tissue mononuclear leukocytes in two subjects dying during the experimental period. The results argue against the hypothesis that lymphoblasts play an important role in dengue virus infection but are consistent with the possibility that mononuclear phagocytes are the site of viral replication in vivo.

摘要

登革2型病毒(D2V)已在培养的灵长类单核吞噬细胞、经丝裂原处理的淋巴细胞和成淋巴细胞样细胞中得到证实。为了确定这些细胞类型中哪一种可能在体内维持感染中起重要作用,九只恒河猴用环磷酰胺进行免疫抑制,然后感染D2V。使白细胞总数维持在低于3000/mm3的维持剂量消除了初次和二次抗体反应。六只成功免疫抑制的动物长时间在血液中循环病毒并感染单核细胞。在实验期间死亡的两名受试者中,从淋巴器官中分离出病毒并在组织单核白细胞中观察到病毒。结果与成淋巴细胞在登革病毒感染中起重要作用的假设相悖,但与单核吞噬细胞是体内病毒复制部位的可能性一致。

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引用本文的文献

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Can non-human primates serve as models for investigating dengue disease pathogenesis?非人灵长类动物能否作为研究登革热疾病发病机制的模型?
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Observations related to pathogenesis of dengue hemorrhagic fever. 3. Virologic studies of fatal disease.与登革出血热发病机制相关的观察。3. 致命疾病的病毒学研究。
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Selective depletion of lymphoid tissue by cyclophosphamide.用环磷酰胺选择性地消耗淋巴组织。
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Immunosuppression and experimental virus infection of the nervous system.免疫抑制与神经系统的实验性病毒感染
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