摘要
M2蛋白通道阻断剂金刚烷胺(amantadine)和金刚乙胺(rimantadine)在体内外均可迅速产生耐药和交叉耐药,机制是源于M2蛋白转膜区突变,涉及的5个主要氨基酸残基是26、27、30、31和34位。神经氨酸酶抑制剂磷酸奥司他韦(oseltamivir)、扎那米韦(zanamivir)和帕那米韦(paramivir)耐药的突变位点发生在病毒A型NA的119、274、292位点及B型152位点。目前尚无一种流感病毒对所有的化疗药物多重耐药。新的神经氨酸酶抑制剂和作用于其他靶点的新药尚处于临床前试验阶段。
Resistance and cross-resistance of influenza A virus to M2 inhibitors adamantane and rimantadine can emerge ra- pidly during treatment in vitro and in vivo. A single point mutation in the codons for amino acids at positions 26, 27, 30, 31, or 34 of the M2 protein can confer the resistance and cross-resistance to both amantadine and rimantadine. Drug resistance emergency in use of neuraminidase （NA） inhibitors, osehamivir, zanamivir and paramivir is caused by the change of the NA at residues 119, 274, 292 （type A） and 152 （type B）. So far no any influenza virus strain has been found to be resistant to all chemotherapeutic drugs. The studies on new NA inhibitors and drugs directed to other targets are now in trial period.
出处
《传染病信息》
2011年第2期124-128,共5页
Infectious Disease Information
关键词
神经氨酸酶
酶抑制剂
抗药性
基因突变
neuraminidase
enzyme inhibitors
drug resistance
gene mutation
