Astrahan Peleg, Arkin Isaiah T
Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences. The Hebrew University of Jerusalem, Edmund J. Safra Campus, Jerusalem 91904, Israel.
Biochim Biophys Acta. 2011 Feb;1808(2):547-53. doi: 10.1016/j.bbamem.2010.06.018. Epub 2010 Jun 27.
The recent outbreaks of avian flu in Southeast Asia and swine flu in Mexico City painfully exemplify the ability of the influenza virus to rapidly mutate and develop resistance to modern medicines. This review seeks to detail the molecular mechanism by which the influenza virus has obtained resistance to amino-adamantyls, one of only two classes of drugs that combat the flu. Amino-adamantyls target the viral M2 H(+) channel and have become largely ineffective due to mutations in the transmembrane domain of the protein. Herein we describe these resistance rendering mutations and the compounded effects they have upon the protein's function and resulting virus viability.
近期东南亚爆发的禽流感以及墨西哥城爆发的猪流感，痛苦地例证了流感病毒迅速变异并对现代药物产生耐药性的能力。本综述旨在详细阐述流感病毒对氨基金刚烷类药物产生耐药性的分子机制，氨基金刚烷类药物是仅有的两类抗流感药物之一。氨基金刚烷类药物作用于病毒的M2 H(+)通道，由于该蛋白跨膜结构域发生突变，这类药物已基本失效。在此，我们描述这些导致耐药性的突变以及它们对蛋白功能和病毒生存能力产生的复合效应。
