Epigenetic Clocks Are Not Accelerated in COVID-19 Patients

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Abstract

Age is a major risk factor for severe outcome of the 2019 coronavirus disease (COVID-19). In this study, we followed the hypothesis that particularly patients with accelerated epigenetic age are affected by severe outcomes of COVID-19. We investigated various DNA methylation datasets of blood samples with epigenetic aging signatures and performed targeted bisulfite amplicon sequencing. Overall, epigenetic clocks closely correlated with the chronological age of patients, either with or without acute respiratory distress syndrome. Furthermore, lymphocytes did not reveal significantly accelerated telomere attrition. Thus, these biomarkers cannot reliably predict higher risk for severe COVID-19 infection in elderly patients.

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  1. SciScore for 10.1101/2020.11.13.20229781: (What is this?)

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

    Table 1: Rigor

    Institutional Review Board Statementnot detected.
    Randomizationnot detected.
    Blindingnot detected.
    Power Analysisnot detected.
    Sex as a biological variablenot detected.

    Table 2: Resources

    No key resources detected.


    Results from OddPub: We did not detect open data. We also did not detect open code. Researchers are encouraged to share open data when possible (see Nature blog).


    Results from LimitationRecognizer: We detected the following sentences addressing limitations in the study:
    Taken together, despite of the limitations of a rather small sample size, our results do not provide evidence that severe outcome of COVID-19 is associated with accelerated epigenetic age or significantly shortened telomere length. Thus, we did not observe signs of premature biological aging in our COVID-19 patients. On the other hand, the infection with SARS-CoV-2 did not directly impact on epigenetic age-predictions. It has recently been demonstrated that HIV infection leads to an average aging advancement of 4.9 years, linking molecular aging, epigenetic regulation and disease progression in this retroviral disease (Gross et al., 2016). Furthermore, coronavirus infections have been suggested to mediate DNA methylation at antigen-presentation-associated gene promoters (Menachery et al., 2018). It is still unclear if the different tissues of a human organism reveal the same pace of epigenetic aging and hence it is conceivable that nasopharyngeal and bronchial epithelium, which is preferentially infected by SARS-CoV-2, reveals higher delta-age with epigenetic age-predictions. A recent study suggested that in airway epithelial cells of healthy controls there is age-associated hypomethylation at a CpG site (cg08559914) located near the transcription start site of the receptor angiotensin-converting enzyme 2 (ACE2) that permits cell entry of SARS-CoV-2 (Corley and Ndhlovu, 2020). Thus, specific age-associated DNA methylations may be functionally relevant to increase susceptibili...

    Results from TrialIdentifier: No clinical trial numbers were referenced.


    Results from Barzooka: We did not find any issues relating to the usage of bar graphs.


    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.
    • Thank you for including a funding statement. Authors are encouraged to include this statement when submitting to a journal.
    • Thank you for including a protocol registration statement.

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