Deep Time Course Proteomics of SARS-CoV- and SARS-CoV-2-Infected Human Lung Epithelial Cells (Calu-3) Reveals Strong Induction of Interferon-Stimulated Gene Expression by SARS-CoV-2 in Contrast to SARS-CoV

  1. Marica Grossegesse
  2. Daniel Bourquain
  3. Markus Neumann
  4. Lars Schaade
  5. Jessica Schulze
  6. Christin Mache
  7. Thorsten Wolff
  8. Andreas Nitsche
  9. Joerg Doellinger

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Abstract

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  1. Version published to 10.1021/acs.jproteome.1c00783
  2. ScreenIT

    SciScore for 10.1101/2021.04.21.440783: (What is this?)

    Please note, not all rigor criteria are appropriate for all manuscripts.

    Table 1: Rigor

    Ethicsnot detected.
    Sex as a biological variablenot detected.
    Randomizationnot detected.
    Blindingnot detected.
    Power Analysisnot detected.
    Cell Line Authenticationnot detected.

    Table 2: Resources

    Experimental Models: Cell Lines
    SentencesResources
    Cell culture and infection: Calu-3 cells (ATCC HTB-55) were cultivated in EMEM containing 10 % FCS, 2 mM L-Gln and non-essential amino acids.
    Calu-3
    suggested: ATCC Cat# HTB-55, RRID:CVCL_0609)
    Software and Algorithms
    SentencesResources
    Gene ontology enrichment of differentially expressed proteins was analysed using the ClueGO app (Version 2.5.7) implemented in Cytoscape (Version 3.8.2) with a Bonferroni-adjusted p-value threshold of 0.05 (12, 17, 18).
    ClueGO
    suggested: (ClueGO, RRID:SCR_005748)
    Cytoscape
    suggested: (Cytoscape, RRID:SCR_003032)

    Results from OddPub: Thank you for sharing your data.

    Results from LimitationRecognizer: We detected the following sentences addressing limitations in the study:
    This meta-analysis demonstrates that proteome coverage is still a limitation which impedes intra-study cross-comparisons due to missing values. Recently, it was proposed that SARS-CoV-2 ORF6 interferes less efficiently with human interferon induction and interferon signalling than SARS-CoV ORF6, which could explain the virus-specific induction of ISG expression and the varying interferon sensitivity (34). The proteome data from this study point towards an additional mechanism. The expression of viral proteins was highly similar between SARS-CoV and SARS-CoV-2 except for the M protein whose expression is enhanced in SARS-CoV. This protein is a component of the viral envelope but its functions beyond are not well characterized. It is known that the homologous M proteins of MERS and SARS-CoV inhibit type I interferon expression (35, 36). Recently, it was discovered that overexpression of the M protein from SARS-CoV-2 in human cells inhibits the production of type I and III IFNs induced by dsRNA-sensing via direct interaction with RIG-I (DDX58) and reduces the induction of ISGs after Sendai virus (SEV) infection and poly (I:C) transfection (33, 37). Additionally, it was shown that the M protein of SARS-CoV inhibits the formation of TRAF3·TANK·TBK1/IKKϵ complex, resulting in the inhibition of IFN transcription (35). We therefore hypothesize that the enhanced expression of the M protein of SARS-CoV reduces the induction of ISG expression in infected cells in comparison to SARS-CoV-...

    Results from TrialIdentifier: No clinical trial numbers were referenced.

    Results from Barzooka: We found bar graphs of continuous data. We recommend replacing bar graphs with more informative graphics, as many different datasets can lead to the same bar graph. The actual data may suggest different conclusions from the summary statistics. For more information, please see Weissgerber et al (2015).

    Results from JetFighter: We did not find any issues relating to colormaps.

    Results from rtransparent:
    • Thank you for including a conflict of interest statement. Authors are encouraged to include this statement when submitting to a journal.
    • No funding statement was detected.
    • No protocol registration statement was detected.

    About SciScore

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  3. Version published to 10.1101/2021.04.21.440783v1 on bioRxiv