Upregulation of HIV-1 replication in chronically infected cells by ingenol derivatives
Upregulation of HIV-1 replication in chronically infected cells by ingenol derivatives
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DOI：
10.1007/s007050050436
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发表时间：
1998-01-01
影响因子：
2.7
通讯作者：
Baba, M
中科院分区：
文献类型：
--
作者：
Fujiwara, M;Okamoto, M;Baba, M
我们以前曾报道，巨大戟二萜醇衍生物是高度有效的抑制人类免疫缺陷病毒I型（HIV-I）在急性感染细胞中的复制。然而，在这项研究中，我们发现一些巨大戟二萜醇衍生物在纳摩尔浓度下强烈增强HIV-1在慢性感染细胞中的复制。其中一种衍生物可以通过激活蛋白激酶C（PKC）激活核因子κ B（NF-κ B B），NF-κ B是HIV-1复制的有效诱导剂。鉴于;另一种既不影响PKC也不影响NF-κ B的衍生物显著增强HIV-1复制，表明在巨大戟醇衍生物诱导的HIV-1上调中也可能存在PKC非依赖性机制。
We have previously reported that ingenol derivatives are highly potent inhibitors of human immunodeficiency virus type I (HIV-I) replication in acutely infected cells. In this study, however, we ha cre found that some ingenol derivatives strongly enhance the replication of HIV-1 in chronically infected cells at nanomolar concentrations. One of the derivatives could activate nuclear factor kappa B(NF-kappa B), a potent inducer of HIV-I replication, through the activation of protein kinase C (PKC). Whereas;another derivative, which affected neither PKC nor NF-kappa B, significantly enhanced HIV-1 replication, suggesting that a PKC-independent mechanism may also exist in ingenol derivative-induced HIV-I up-regulation.