DAILAB, Department of Biochemical Engineering and Biotechnology, Indian Institute of Technology (IIT) Delhi, Hauz Khas, New Delhi 110016, India.
AIST-India DAILAB, DBT-AIST International Center for Translational and Environmental Research (DAICENTER), National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba 3058565, Japan.
Biosci Rep. 2021 Oct 29;41(10). doi: 10.1042/BSR20212156.
Coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has become a global health emergency. Although new vaccines have been generated and being implicated, discovery and application of novel preventive and control measures are warranted. We aimed to identify compounds that may possess the potential to either block the entry of virus to host cells or attenuate its replication upon infection. Using host cell surface receptor expression (angiotensin-converting enzyme 2 (ACE2) and Transmembrane protease serine 2 (TMPRSS2)) analysis as an assay, we earlier screened several synthetic and natural compounds and identified candidates that showed ability to down-regulate their expression. Here, we report experimental and computational analyses of two small molecules, Mortaparib and MortaparibPlus that were initially identified as dual novel inhibitors of mortalin and PARP-1, for their activity against SARS-CoV-2. In silico analyses showed that MortaparibPlus, but not Mortaparib, stably binds into the catalytic pocket of TMPRSS2. In vitro analysis of control and treated cells revealed that MortaparibPlus caused down-regulation of ACE2 and TMPRSS2; Mortaparib did not show any effect. Furthermore, computational analysis on SARS-CoV-2 main protease (Mpro) that also predicted the inhibitory activity of MortaparibPlus. However, cell-based antiviral drug screening assay showed 30-60% viral inhibition in cells treated with non-toxic doses of either MortaparibPlus or Mortaparib. The data suggest that these two closely related compounds possess multimodal anti-COVID-19 activities. Whereas MortaparibPlus works through direct interactions/effects on the host cell surface receptors (ACE2 and TMPRSS2) and the virus protein (Mpro), Mortaparib involves independent mechanisms, elucidation of which warrants further studies.
新型冠状病毒病(COVID-19)大流行是由严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)病毒引起的,已成为全球卫生紧急事件。尽管已经产生了新的疫苗并正在进行研究,但仍需要发现和应用新的预防和控制措施。我们旨在确定可能具有阻止病毒进入宿主细胞或减轻感染后复制能力的化合物。我们使用宿主细胞表面受体表达(血管紧张素转换酶 2(ACE2)和跨膜丝氨酸蛋白酶 2(TMPRSS2))分析作为检测方法,早期筛选了几种合成和天然化合物,并确定了具有下调其表达能力的候选化合物。在这里,我们报告了两种小分子化合物(Mortaparib 和 MortaparibPlus)的实验和计算分析,它们最初被鉴定为 mortalin 和 PARP-1 的双重新型抑制剂,用于研究其对 SARS-CoV-2 的活性。计算机分析表明,MortaparibPlus 而不是 Mortaparib 稳定地结合到 TMPRSS2 的催化口袋中。对照和处理细胞的体外分析表明,MortaparibPlus 导致 ACE2 和 TMPRSS2 的下调;Mortaparib 没有显示任何效果。此外,对 SARS-CoV-2 主要蛋白酶(Mpro)的计算分析也预测了 MortaparibPlus 的抑制活性。然而,基于细胞的抗病毒药物筛选试验表明,用非毒性剂量的 MortaparibPlus 或 Mortaparib 处理的细胞中病毒抑制率为 30-60%。数据表明,这两种密切相关的化合物具有多种抗 COVID-19 活性。MortaparibPlus 通过直接作用于宿主细胞表面受体(ACE2 和 TMPRSS2)和病毒蛋白(Mpro)发挥作用,而 Mortaparib 则涉及独立的机制,进一步研究需要阐明这些机制。