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Repurposing existing drugs approved for other conditions is crucial to identifying speci c therapeutics against SARS-CoV-2 causing COVID-19 (coronavirus disease-2019) pandemic. Towards this attempt, it is important to understand how this virus hijacks the host system during the course of infection and determine potential virus-and host-targeted inhibitors. This study elucidates the underlying virus-host interaction based on differentially expressed gene pro ling, functional enrichment and pathway analysis, protein-protein and protein-drug interactions utilizing the information on transcriptional response to SARS-CoV-2 infection from GSE 147507 dataset containing COVID-19 case relative to healthy control and infected cell culture compared to uninfected one. Low IFN signaling, chemokines level elevation, and proin ammatory cytokines release were observed markedly. We identi ed MYC-rapamycin and ABCG2rapamycin interactions, and unique gene signatures in case (regulation of protein modi cation and MAPK signaling) as well as in cell (metabolic dysregulation and interferon signaling) different from known COVID-19 genes. Highlights Low IFN signaling, chemokines level elevation, and proin ammatory cytokines release were observed markedly Cyclosporine, doxycycline, chloroquine, rapamycin interacted with MYC, PPP3R1, FOS, ABCG2, TNF in case and culture Cyclosporine, azithromycin, rapamycin, oseltamivir interacted with IL6, CD8A, CD40LG, IL10, CSF3 known COVID-19 genes Chloroquine, lopinavir, ritonavir, interferon beta-1a antagonist are included in WHO solidarity trial for COVID-19 Among a plethora of repurposable drugs those appearing here with unique gene signatures might be

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Japan introduced a Helicobacter pylori eradication therapy strategy in 2013, with the aim of decreasing the number of gastric cancer‐related death, the number of new cases of gastric cancer, and associated medical costs. Five years have passed since then, but no reduction in the annual number of gastric cancer has been observed. In addition, it was suggested that the number of deaths due to gastric cancer could be reduced to 30,000 a year by 2020, but the annual death toll in 2017 remained at more than 45,000. Based on the above evidence, it was examined whether it was possible to reach the target value based on the data from the last 5 years. The number of deaths per year in 2020 is predicted to be more than 40,000, which is clearly different from the target value. Logically, the effect of the strategy might appear by 2023. However, there is a possibility that the risk of gastric cancer may increase in some populations due to the influence of proton pump inhibitors and dysbiosis in the gastric microbiome. To solve these problems, combined therapy with PPIs and aspirin for patients after H pylori eradication should be considered.

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