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  • Structural and functional conservation of the programmed -1 ribosomal frameshift signal of SARS coronavirus 2 (SARS-CoV-2) #MMPMID32571880
  • Kelly JA; Olson AN; Neupane K; Munshi S; San Emeterio J; Pollack L; Woodside MT; Dinman JD
  • J Biol Chem 2020[Jul]; 295 (31): 10741-10748 PMID32571880show ga
  • Approximately 17 years after the severe acute respiratory syndrome coronavirus (SARS-CoV) epidemic, the world is currently facing the COVID-19 pandemic caused by SARS corona virus 2 (SARS-CoV-2). According to the most optimistic projections, it will take more than a year to develop a vaccine, so the best short-term strategy may lie in identifying virus-specific targets for small molecule-based interventions. All coronaviruses utilize a molecular mechanism called programmed -1 ribosomal frameshift (-1 PRF) to control the relative expression of their proteins. Previous analyses of SARS-CoV have revealed that it employs a structurally unique three-stemmed mRNA pseudoknot that stimulates high -1 PRF rates and that it also harbors a -1 PRF attenuation element. Altering -1 PRF activity impairs virus replication, suggesting that this activity may be therapeutically targeted. Here, we comparatively analyzed the SARS-CoV and SARS-CoV-2 frameshift signals. Structural and functional analyses revealed that both elements promote similar -1 PRF rates and that silent coding mutations in the slippery sites and in all three stems of the pseudoknot strongly ablate -1 PRF activity. We noted that the upstream attenuator hairpin activity is also functionally retained in both viruses, despite differences in the primary sequence in this region. Small-angle X-ray scattering analyses indicated that the pseudoknots in SARS-CoV and SARS-CoV-2 have the same conformation. Finally, a small molecule previously shown to bind the SARS-CoV pseudoknot and inhibit -1 PRF was similarly effective against -1 PRF in SARS-CoV-2, suggesting that such frameshift inhibitors may be promising lead compounds to combat the current COVID-19 pandemic.
  • |*Drug Design[MESH]
  • |Betacoronavirus/chemistry/*genetics[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*drug therapy[MESH]
  • |Frameshifting, Ribosomal/*drug effects[MESH]
  • |Gene Expression Regulation, Viral[MESH]
  • |Humans[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*drug therapy[MESH]
  • |RNA, Viral/chemistry/*genetics[MESH]
  • |SARS-CoV-2[MESH]
  • |Virus Replication/drug effects[MESH]

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  • suck abstract from ncbi

    10741 31.295 2020