Measles Virus Fusion Protein: Structure, Function and Inhibition.
Measles Virus Fusion Protein: Structure, Function and Inhibition.
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DOI：
10.3390/v8040112
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发表时间：
2016-04-21
期刊：
影响因子：
--
通讯作者：
Aguilar HC
中科院分区：
文献类型：
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作者：
Plattet P;Alves L;Herren M;Aguilar HC
麻疹病毒（MeV）是副粘病毒科的一种高传染性成员，可引起人类麻疹。负单链包膜病毒的副粘病毒科家族包括几种重要的人类和动物病原体，MeV每年造成约120，000人死亡。MeV和犬瘟热病毒（CDV）介导的疾病可以通过接种疫苗预防。然而，次优的疫苗输送继续助长MeV爆发。抗病毒药物暴露后预防已被提出作为一种新的战略，以补充疫苗接种计划，填补群体免疫差距。最近的研究表明，麻疹病毒糖蛋白诱导的膜融合是病毒进入和感染的第一个关键步骤，并决定细胞病理和疾病的结果。我们对麻疹病毒相关膜融合的分子理解已经朝着通过用抑制性分子处理融合糖蛋白来控制这一过程的可行性取得了很大进展。目前开发抗膜融合药物的方法和我们对耐药机制的了解强烈表明，联合治疗将是一个先决条件。因此，发现额外的抗融合和/或抗附着蛋白小分子化合物可能最终转化为现实的治疗选择。
Measles virus (MeV), a highly contagious member of the Paramyxoviridae family, causes measles in humans. The Paramyxoviridae family of negative single-stranded enveloped viruses includes several important human and animal pathogens, with MeV causing approximately 120,000 deaths annually. MeV and canine distemper virus (CDV)-mediated diseases can be prevented by vaccination. However, sub-optimal vaccine delivery continues to foster MeV outbreaks. Post-exposure prophylaxis with antivirals has been proposed as a novel strategy to complement vaccination programs by filling herd immunity gaps. Recent research has shown that membrane fusion induced by the morbillivirus glycoproteins is the first critical step for viral entry and infection, and determines cell pathology and disease outcome. Our molecular understanding of morbillivirus-associated membrane fusion has greatly progressed towards the feasibility to control this process by treating the fusion glycoprotein with inhibitory molecules. Current approaches to develop anti-membrane fusion drugs and our knowledge on drug resistance mechanisms strongly suggest that combined therapies will be a prerequisite. Thus, discovery of additional anti-fusion and/or anti-attachment protein small-molecule compounds may eventually translate into realistic therapeutic options.