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MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

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    The translational landscape of SARS-CoV-2 and infected cells

    Authors: Maritza Puray-Chavez; Kasyap Tenneti; Hung R. Vuong; Nakyung Lee; Yating Liu; Amjad Horani; Tao Huang; James B. Case; Wei Yang; Michael S. Diamond; Steven L. Brody; Joseph Dougherty; Sebla B. Kutluay; Aniket S Rali; Leo Simpson; Mehrdad Saririan; Dan Hobohm; W. Tom Stump; James A Fitzpatrick; Xuping Xie; Pei-Yong Shi; J Travis Hinson; Weng-Tein Gi; Constanze Schmidt; Florian Leuschner; Chieh-Yu Lin; Michael S Diamond; Michael J Greenberg; Kory J Lavine; Pamela J. Bjorkman; Saurabh Mehandru; Paul D. Bieniasz; Marina Caskey; Michel C. Nussenzweig

    doi:10.1101/2020.11.03.367516 Date: 2020-11-05 Source: bioRxiv

    SARS-CoV-2, a betacoronavirus with a positive-sense RNA genome, has caused the ongoing COVID-19 pandemic MESHD COVID-19 pandemic MESHD. Although a large number of transcriptional profiling studies have been conducted in SARS-CoV-2 infected MESHD cells, little is known regarding the translational landscape of host and viral proteins. Here, using ribosome profiling in SARS-CoV-2-infected MESHD cells, we identify structural elements that regulate viral gene expression, alternative translation initiation events, as well as host responses regulated by mRNA translation. We found that the ribosome density was low within the SARS-CoV-2 frameshifting element but high immediately downstream, which suggests the utilization of a highly efficient ribosomal frameshifting strategy. In SARS-CoV-2-infected cells, although many chemokine, cytokine and interferon HGNC stimulated genes were upregulated at the mRNA level, they were not translated efficiently, suggesting a translational block that disarms host innate host responses. Together, these data reveal the key role of mRNA translation in SARS-CoV-2 replication and highlight unique mechanisms for therapeutic development.

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MeSH Disease
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SARS-CoV-2 Proteins


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