Antiviral efficacy in vivo of the anti-human immunodeficiency virus bicyclam SDZ SID 791 (JM 3100), an inhibitor of infectious cell entry
Antiviral efficacy in vivo of the anti-human immunodeficiency virus bicyclam SDZ SID 791 (JM 3100), an inhibitor of infectious cell entry
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DOI：
10.1128/aac.40.3.750
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发表时间：
1996-03-01
影响因子：
4.9
通讯作者：
McCune, JM
中科院分区：
文献类型：
--
作者：
Datema, R;Rabin, L;McCune, JM
SID 791 是一种 Bicyclam，通过阻止病毒进入细胞来抑制人类免疫缺陷病毒 (HIV) 体外复制，是 HIV 1 型感染 SCID-hu Thy/Liv 小鼠中病毒产生和人类 CD4(+) T 细胞耗竭的有效抑制剂。血浆中每毫升 100 纳克 SID 791 或更高的稳定水平可对 p24 抗原形成产生统计学上显着的抑制。每日注射 SID 791 导致病毒血症呈剂量依赖性下降，并且这种抑制作用可以通过齐多夫定或去达诺糖的共同给药来增强。目前的研究表明，SID 791 单独使用或与许可的抗病毒药物联合使用可能会降低 HIV 感染患者的病毒载量，并且推而广之，感染性细胞进入步骤是 HN 疾病抗病毒化疗的有效靶标。 SCID-hu Thy/Liv 模型实际上提供了一种快速方法来评估具有新型抗病毒作用模式的化合物的潜力以及抗病毒药物组合的潜力。
SID 791, a bicyclam inhibiting human immunodeficiency virus (HIV) replication in vitro by blocking virus entry into cells, is an effective inhibitor of virus production and of depletion of human CD4(+) T cells in HIV type 1-infected SCID-hu Thy/Liv mice. Steady levels of 100 ng of SID 791 or higher per mi in plasma resulted in statistically significant inhibition of p24 antigen formation. Daily injections of SID 791 caused a dose-dependent decrease in viremia, and this inhibition could be potentiated by coadministration of zidovudine or didanose. The present study suggests that SID 791 alone or in combination with licensed antiviral agents may decrease the virus load in HIV-infected patients and, by extension, that the infectious cell entry step is a valid target for antiviral chemotherapy of HN disease. The SCID-hu Thy/Liv model in effect provides a rapid means of assessing the potential of compounds with novel modes of antiviral action, as well as the potential of antiviral drug combinations.