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Omicron SARS-CoV-2/hACE2 的结构适应:进化驱动力的生物物理起源。

Structure adaptation in Omicron SARS-CoV-2/hACE2: Biophysical origins of evolutionary driving forces.

机构信息

The Hartree Centre, STFC Daresbury Laboratory, Warrington, United Kingdom; Scientific Computing Department, STFC Daresbury Laboratory, Warrington, United Kingdom.

The Hartree Centre, STFC Daresbury Laboratory, Warrington, United Kingdom.

出版信息

Biophys J. 2023 Oct 17;122(20):4057-4067. doi: 10.1016/j.bpj.2023.09.003. Epub 2023 Sep 16.

Abstract

Since its emergence, the COVID-19 threat has been sustained by a series of transmission waves initiated by new variants of the SARS-CoV-2 virus. Some of these arise with higher transmissivity and/or increased disease severity. Here, we use molecular dynamics simulations to examine the modulation of the fundamental interactions between the receptor binding domain (RBD) of the spike glycoprotein and the host cell receptor (human angiotensin-converting enzyme 2 [hACE2]) arising from Omicron variant mutations (BA.1 and BA.2) relative to the original wild-type strain. Our key findings are that glycans play a vital role at the RBD···hACE2 interface for the Omicrons, and the interplay between glycans and sequence mutations leads to enhanced binding. We find significant structural differences in the complexes, which overall bring the spike protein and its receptor into closer proximity. These are consistent with and attributed to the higher positive charge on the RBD conferred by BA.1 and BA.2 mutations relative to the wild-type. However, further differences between subvariants BA.1 and BA.2 (which have equivalent RBD charges) are also evident: mutations reduce interdomain interactions between the up chain and its clockwise neighbor chain in particular for the latter, resulting in enhanced flexibility for BA.2. Consequently, we see occurrence of additional close contacts in one replica of BA.2, which include binding to hACE2 by a second RBD in addition to the up chain. Although this motif is not seen in BA.1, we find that the Omicrons can directly/indirectly bind a down-RBD to hACE2 through glycans: the role of the glycan on N90 of hACE2 switches from inhibiting to facilitating the binding to Omicron spike protein via glycan-protein lateral interactions. These structural and electrostatic differences offer further insight into the mechanisms by which viral mutations modulate host cell binding and provide a biophysical basis for evolutionary driving forces.

摘要

自出现以来,COVID-19 威胁一直持续受到 SARS-CoV-2 病毒新变体引发的一系列传播波的推动。其中一些变体具有更高的传染性和/或增加疾病的严重程度。在这里,我们使用分子动力学模拟来研究奥密克戎变体突变(BA.1 和 BA.2)相对于原始野生型菌株引起的刺突糖蛋白受体结合域(RBD)与宿主细胞受体(人血管紧张素转换酶 2 [hACE2])之间基本相互作用的调制。我们的主要发现是糖基在奥密克戎的 RBD···hACE2 界面中起着至关重要的作用,糖基和序列突变之间的相互作用导致结合增强。我们发现复合物存在显著的结构差异,总体上使刺突蛋白及其受体更加接近。这与 BA.1 和 BA.2 突变赋予 RBD 的更高正电荷相一致,并归因于更高的正电荷。然而,BA.1 和 BA.2 亚变体(具有等效的 RBD 电荷)之间也存在进一步的差异:突变特别是对于后者,减少了上链与其顺时针相邻链之间的结构域间相互作用,导致 BA.2 的灵活性增强。因此,我们在 BA.2 的一个副本中看到了额外的紧密接触的发生,其中包括上链与 hACE2 的结合,以及除上链外的第二个 RBD 与 hACE2 的结合。虽然这种模体在 BA.1 中没有看到,但我们发现奥密克戎可以通过糖基直接/间接将下 RBD 与 hACE2 结合:hACE2 上 N90 的糖基的作用从抑制转变为通过糖基-蛋白侧向相互作用促进与奥密克戎刺突蛋白的结合。这些结构和静电差异为病毒突变调节宿主细胞结合的机制提供了进一步的见解,并为进化驱动力提供了生物物理基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc5/10624932/7fa0eb2c2f88/gr1.jpg

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