The current pandemic of 2019 novel coronavirus disease (COVID-19) caused by a novel virus strain, 2019-nCoV/SARS-CoV-2 have posed a serious threat to global public health and economy. It is largely unknown how the human immune system responds to this infection. A better understanding of the immune response to SARS-CoV-2 will be important to develop therapeutics against COVID-19. Here, we have used transcriptomic profile of human alveolar adenocarcinoma cells (A549) infected with SARS-CoV-2 and employed a network biology approach to generate human-virus interactome. Network topological analysis discovers 15 SARS-CoV-2 targets, which belongs to a subset of interferon (IFN) stimulated genes (ISGs). These ISGs (IFIT1, IFITM1, IRF7, ISG15, MX1, and OAS2) can be considered as potential candidates for drug targets in the treatments of COVID-19. We have identified significant interaction between ISGs and TLR3 agonists, like poly I: C, and imiquimod, and suggests that TLR3 agonists can be considered as a potential drug for drug repurposing in COVID-19. Our network centric analysis suggests that moderating the innate immune response is a valuable approach to target COVID-19.

当前由一种新型病毒株2019-nCoV / SARS-CoV-2引起的2019年新型冠状病毒疾病（COVID-19）大流行对全球公共卫生和经济构成了严重威胁。人体免疫系统如何应对这种感染在很大程度上是未知的。更好地理解对SARS-CoV-2的免疫反应对于开发针对COVID-19的疗法非常重要。在这里，我们使用了感染SARS-CoV-2的人肺泡腺癌细胞（A549）的转录组谱，并采用了网络生物学方法来生成人病毒相互作用组。网络拓扑分析发现了15个SARS-CoV-2靶标，该靶标属于干扰素（IFN）刺激基因（ISG）的子集。这些ISG（IFIT1，IFITM1，IRF7，ISG15，MX1和OAS2）可以被视为COVID-19治疗药物靶标的潜在候选者。我们已经确定ISG和TLR3激动剂（例如聚I：C和咪喹莫特）之间存在显着的相互作用，并建议TLR3激动剂可被视为COVID-19中潜在的药物重新用途。我们以网络为中心的分析表明，减轻先天免疫应答是靶向COVID-19的宝贵方法。