Genome Biology Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
Department of Infectious Diseases, Molecular Virology, Heidelberg University Hospital, Heidelberg, Germany.
Mol Syst Biol. 2021 Feb;17(2):e10188. doi: 10.15252/msb.202010188.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a global threat to human health and has compromised economic stability. In addition to the development of an effective vaccine, it is imperative to understand how SARS-CoV-2 hijacks host cellular machineries on a system-wide scale so that potential host-directed therapies can be developed. In situ proteome-wide abundance and thermal stability measurements using thermal proteome profiling (TPP) can inform on global changes in protein activity. Here we adapted TPP to high biosafety conditions amenable to SARS-CoV-2 handling. We discovered pronounced temporal alterations in host protein thermostability during infection, which converged on cellular processes including cell cycle, microtubule and RNA splicing regulation. Pharmacological inhibition of host proteins displaying altered thermal stability or abundance during infection suppressed SARS-CoV-2 replication. Overall, this work serves as a framework for expanding TPP workflows to globally important human pathogens that require high biosafety containment and provides deeper resolution into the molecular changes induced by SARS-CoV-2 infection.
严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)是对人类健康的全球性威胁,并破坏了经济稳定。除了开发有效的疫苗外,了解 SARS-CoV-2 如何在全系统范围内劫持宿主细胞机制至关重要,以便能够开发潜在的宿主导向疗法。使用热蛋白质组学 profiling(TPP)进行原位蛋白质组学广泛性丰度和热稳定性测量可以提供有关蛋白质活性的全局变化的信息。在这里,我们适应了 TPP 以适应 SARS-CoV-2 处理的高生物安全条件。我们发现感染过程中宿主蛋白热稳定性发生了明显的时间变化,这些变化集中在包括细胞周期,微管和 RNA 剪接调控在内的细胞过程上。在感染过程中抑制显示出热稳定性或丰度改变的宿主蛋白的药理学抑制可以抑制 SARS-CoV-2 的复制。总的来说,这项工作为将 TPP 工作流程扩展到需要高生物安全控制的全球重要人类病原体提供了框架,并为 SARS-CoV-2 感染引起的分子变化提供了更深入的分辨率。