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10.1002/2211-5463.13413

http://scihub22266oqcxt.onion/10.1002/2211-5463.13413
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35429230!9110871!35429230
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suck abstract from ncbi


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pmid35429230      FEBS+Open+Bio 2022 ; 12 (9): 1584-1601
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  • Viral and cellular translation during SARS-CoV-2 infection #MMPMID35429230
  • Eriani G; Martin F
  • FEBS Open Bio 2022[Sep]; 12 (9): 1584-1601 PMID35429230show ga
  • SARS-CoV-2 is a betacoronavirus that emerged in China in December 2019 and which is the causative agent of the Covid-19 pandemic. This enveloped virus contains a large positive-sense single-stranded RNA genome. In this review, we summarize the current knowledge on the molecular mechanisms for the translation of both viral transcripts and cellular messenger RNAs. Non-structural proteins are encoded by the genomic RNA and are produced in the early steps of infection. In contrast, the structural proteins are produced from subgenomic RNAs that are translated in the late phase of the infectious program. Non-structural protein 1 (NSP1) is a key molecule that regulates both viral and cellular translation. In addition, NSP1 interferes with multiple steps of the interferon I pathway and thereby blocks host antiviral responses. Therefore, NSP1 is a drug target of choice for the development of antiviral therapies.
  • |*COVID-19[MESH]
  • |Antiviral Agents/therapeutic use[MESH]
  • |Humans[MESH]
  • |Pandemics[MESH]
  • |RNA, Messenger/genetics[MESH]
  • |SARS-CoV-2[MESH]


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