PMC:7073332 / 21354-22886 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":"Selective estrogen receptor modulators\nAn overexpression of estrogen receptor has been shown to play a crucial role in inhibiting viral replication37. Selective estrogen receptor modulators (SERMs) have been reported to play a broader role in inhibiting viral replication through the non-classical pathways associated with estrogen receptor37. SERMs interfere at the post viral entry step and affect the triggering of fusion, as the SERMs’ antiviral activity still can be observed in the absence of detectable estrogen receptor expression18. Toremifene (Z = –3.23, Fig. 5a), the first generation of nonsteroidal SERM, exhibits potential effects in blocking various viral infections, including MERS-CoV, SARS-CoV, and Ebola virus in established cell lines17,38. Compared to the classical ESR1-related antiviral pathway, toremifene prevents fusion between the viral and endosomal membrane by interacting with and destabilizing the virus membrane glycoprotein, and eventually inhibiting viral replication39. As shown in Fig. 5b, toremifene potentially affects several key host proteins associated with HCoV, such as RPL19, HNRNPA1, NPM1, EIF3I, EIF3F, and EIF3E40,41. Equilin (Z = –2.52 and GSEA score = 3), an estrogenic steroid produced by horses, also has been proven to have moderate activity in inhibiting the entry of Zaire Ebola virus glycoprotein and human immunodeficiency virus (ZEBOV-GP/HIV)18. Altogether, network-predicted SERMs (such as toremifene and equilin) offer candidate repurposable drugs for 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