PMC:7073332 / 4808-6198 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7073332","sourcedb":"PMC","sourceid":"7073332","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7073332","text":"Viruses (including HCoV) require host cellular factors for successful replication during infection1. Systematic identification of virus–host protein–protein interactions (PPIs) offers an effective way toward elucidating the mechanisms of viral infection15,16. Subsequently, targeting cellular antiviral targets, such as virus–host interactome, may offer a novel strategy for the development of effective treatments for viral infections1, including SARS-CoV17, MERS-CoV17, Ebola virus18, and Zika virus14,19–21. We recently presented an integrated antiviral drug discovery pipeline that incorporated gene-trap insertional mutagenesis, known functional drug–gene network, and bioinformatics analyses14. This methodology allows to identify several candidate repurposable drugs for Ebola virus11,14. Our work over the last decade has demonstrated how network strategies can, for example, be used to identify effective repurposable drugs13,22–27 and drug combinations28 for multiple human diseases. For example, network-based drug–disease proximity sheds light on the relationship between drugs (e.g., drug targets) and disease modules (molecular determinants in disease pathobiology modules within the PPIs), and can serve as a useful tool for efficient screening of potentially new indications for approved drugs, as well as drug combinations, as demonstrated in our recent 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