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抗移联体降低了SARS病毒的形状可塑性伪结节

Dustin B Ritchie¹, Jingchyuan Soong, William K A Sikkema

¹Department of Physics, University of Alberta , Edmonton, Alberta T6G 2E1, Canada.

Journal of the American Chemical Society

|January 23, 2014

概括

一个反移联体抑制了SARS伪节点的形态可塑性,防止了替代形态变体的形成. 这一发现将伪结的动态与被编程的核糖体框架转移联系在一起,这表明新的抗病毒药物点.

科学领域:

分子生物学分子生物学
病毒学病毒学
生物物理学的生物物理.

背景情况:

编程的-1核糖体框架转移 (-1PRF) 对于病毒基因表达至关重要.
mRNA伪结刺激-1PRF,使它们成为潜在的抗病毒点.
伪结结诱导的-1 PRF的确切机制是有争议的,模型侧重于形状可塑性.

研究的目的:

为了研究构造性可塑性在联结型伪结中所起的作用.
为了确定一个反位转移连接体是否会影响伪结的动力学和-1 PRF效率.
探索针对抗病毒药物设计的伪结合形态动态的潜力.

主要方法:

利用单分子力光谱学以机械地展开SARS-CoV伪结.
测量了一种已确定的反变位连接体对伪结的形状动态的影响.
评估了联体诱导的形状可塑性变化与-1 PRF效率之间的相关性.

主要成果:

对SARS伪结节的带结合显著降低了其形状可塑性.
在联结结合后,取消了替代伪结合体的形成.
这种抑制形状动态与降低-1 PRF效率相关.

结论:

证实了伪节点形状可塑性和-1 PRF效率之间的联系.
证明了一种反移联体破坏了伪结的动态.
表明,准伪节形态动态是一种可行的抗病毒药物策略.

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