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10.1073/pnas.2023051118

http://scihub22266oqcxt.onion/10.1073/pnas.2023051118
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34185680!8256030!34185680
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suck abstract from ncbi


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pmid34185680      Proc+Natl+Acad+Sci+U+S+A 2021 ; 118 (26): ä
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  • Restriction of SARS-CoV-2 replication by targeting programmed -1 ribosomal frameshifting #MMPMID34185680
  • Sun Y; Abriola L; Niederer RO; Pedersen SF; Alfajaro MM; Silva Monteiro V; Wilen CB; Ho YC; Gilbert WV; Surovtseva YV; Lindenbach BD; Guo JU
  • Proc Natl Acad Sci U S A 2021[Jun]; 118 (26): ä PMID34185680show ga
  • Translation of open reading frame 1b (ORF1b) in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) requires a programmed -1 ribosomal frameshift (-1 PRF) promoted by an RNA pseudoknot. The extent to which SARS-CoV-2 replication may be sensitive to changes in -1 PRF efficiency is currently unknown. Through an unbiased, reporter-based high-throughput compound screen, we identified merafloxacin, a fluoroquinolone antibacterial, as a -1 PRF inhibitor for SARS-CoV-2. Frameshift inhibition by merafloxacin is robust to mutations within the pseudoknot region and is similarly effective on -1 PRF of other betacoronaviruses. Consistent with the essential role of -1 PRF in viral gene expression, merafloxacin impedes SARS-CoV-2 replication in Vero E6 cells, thereby providing proof-of-principle for targeting -1 PRF as a plausible and effective antiviral strategy for SARS-CoV-2 and other coronaviruses.
  • |Animals[MESH]
  • |Antiviral Agents/*pharmacology[MESH]
  • |Betacoronavirus[MESH]
  • |Chlorocebus aethiops[MESH]
  • |Fluoroquinolones/pharmacology[MESH]
  • |Frameshifting, Ribosomal/*drug effects/genetics[MESH]
  • |Mutation[MESH]
  • |Nucleic Acid Conformation[MESH]
  • |RNA, Viral/chemistry/genetics[MESH]
  • |SARS-CoV-2/*drug effects/physiology[MESH]
  • |Vero Cells[MESH]


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