Ion transport blockers inhibit human rhinovirus 2 release
Ion transport blockers inhibit human rhinovirus 2 release
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DOI：
10.1016/j.antiviral.2005.05.003
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发表时间：
2005-08-01
影响因子：
7.6
通讯作者：
Petrou, S
中科院分区：
文献类型：
--
作者：
Gazina, EV;Harrison, DN;Petrou, S
微小核糖核酸病毒复制导致细胞质K+外漏以及Na+和Ca~(2+)内流。在这项研究中，我们探索了阻断钙和钠离子内流将减少鼻病毒产生和/或释放的可能性。钙通道阻滞剂维拉帕米和地尔硫卓，以及Na+/H+交换阻断剂和上皮Na‘通道阻断剂EIPA，都能抑制病毒的产生和释放。对病毒释放的影响比对产量的影响更明显，因此增加了鼻病毒释放可能成为抗病毒药物的靶点的可能性。出乎意料的是，我们的结果还表明，钙通道阻滞剂的抗病毒活性并不是由于阻断了钙内流。同样，EIPA的抗病毒活性似乎与阻断细胞内Na+/H+交换或上皮Na+通道无关。讨论了这些化合物抗病毒活性的潜在替代机制。(C)2005 Elsevier B.V.保留所有权利。
Picornavirus replication causes leakage of cytoplasmic K+ and an influx of Na+ and Ca2+. In this study, we have explored the possibility that a blockade of Ca2+ and Na+ influx would reduce rhinovirus production and/or release. The Ca2+-channel blockers, verapamil and diltiazem, as well as the blocker of Na+/H+ exchange and the epithelial Na' channel, EIPA, inhibited both virus production and release. The effect on vir-us release was more pronounced than the effect on production, thus raising the possibility that rhinovirus release may serve as a target for antiviral agents. Unexpectedly, our results also showed that the antiviral activity of the Ca2+-channel blockers was not due to the block of Ca2+ influx. Similarly, the antiviral activity of EIPA appeared to be unrelated to the blockade of cellular Na+/H+ exchanger or the epithelial Na+ channel. Potential alternative mechanisms of the antiviral activity of these compounds are discussed. (c) 2005 Elsevier B.V. All rights reserved.