SARS-CoV-2 (COVID-19) by the numbers

  1. Yinon M Bar-On
  2. Avi Flamholz
  3. Rob Phillips
  4. Ron Milo  Is a corresponding author
  1. The Weizmann Institute for Science, Israel
  2. University of California, Berkeley, United States
  3. California Institute of Technology, United States

Abstract

The current SARS-CoV-2 pandemic is a harsh reminder of the fact that, whether in a single human host or a wave of infection across continents, viral dynamics is often a story about the numbers. In this snapshot, our aim is to provide a one-stop, curated graphical source for the key numbers that help us understand the virus driving our current global crisis. The discussion is framed around two broad themes: 1) the biology of the virus itself and 2) the characteristics of the infection of a single human host. Our one-page summary provides the key numbers pertaining to SARS-CoV-2, based mostly on peer-reviewed literature. The numbers reported in summary format are substantiated by the annotated references below. Readers are urged to remember that much uncertainty remains and knowledge of this pandemic and the virus driving it is rapidly evolving. In the paragraphs below we provide 'back of the envelope' calculations that exemplify the insights that can be gained from knowing some key numbers and using quantitative logic. These calculations serve to improve our intuition through sanity checks, but do not replace detailed epidemiological analysis.

Data availability

This article is a compilation of previously published data; no new data were generated in this study.

Article and author information

Author details

  1. Yinon M Bar-On

    Department of Plant and Environmental Sciences, The Weizmann Institute for Science, Rehovot, Israel
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-8477-609X
  2. Avi Flamholz

    Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-9278-5479
  3. Rob Phillips

    Department of Bioengineering, California Institute of Technology, Pasadena, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-3082-2809
  4. Ron Milo

    Department of Plant and Environmental Sciences, The Weizmann Institute for Science, Rehovot, Israel
    For correspondence
    ron.milo@weizmann.ac.il
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-1641-2299

Funding

National Institutes of Health (1R35 GM118043-01 (Maximizing Investigators Research Award))

  • Rob Phillips

Charles and Louise Gartner professional chair

  • Ron Milo

Azrieli Fellow

  • Yinon M Bar-On

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Michael B Eisen, HHMI, University of California, Berkeley, United States

Publication history

  1. Received: March 27, 2020
  2. Accepted: March 30, 2020
  3. Accepted Manuscript published: March 31, 2020 (version 1)
  4. Accepted Manuscript updated: April 1, 2020 (version 2)
  5. Accepted Manuscript updated: April 2, 2020 (version 3)
  6. Version of Record published: May 14, 2020 (version 4)

Copyright

© 2020, Bar-On et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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  1. Yinon M Bar-On
  2. Avi Flamholz
  3. Rob Phillips
  4. Ron Milo
(2020)
SARS-CoV-2 (COVID-19) by the numbers
eLife 9:e57309.
https://doi.org/10.7554/eLife.57309
  1. Further reading

Further reading

    1. Epidemiology and Global Health
    Tianyi Huang
    Insight

    A large observational study has found that irregular sleep-wake patterns are associated with a higher risk of overall mortality, and also mortality from cancers and cardiovascular disease.

    1. Epidemiology and Global Health
    Lachlan Cribb, Ramon Sha ... Matthew P Pase
    Research Article

    Background:

    Irregular sleep-wake timing may cause circadian disruption leading to several chronic age-related diseases. We examined the relationship between sleep regularity and risk of all-cause, cardiovascular disease (CVD), and cancer mortality in 88,975 participants from the prospective UK Biobank cohort.

    Methods:

    The sleep regularity index (SRI) was calculated as the probability of an individual being in the same state (asleep or awake) at any two time points 24 hr apart, averaged over 7 days of accelerometry (range 0–100, with 100 being perfectly regular). The SRI was related to the risk of mortality in time-to-event models.

    Results:

    The mean sample age was 62 years (standard deviation [SD], 8), 56% were women, and the median SRI was 60 (SD, 10). There were 3010 deaths during a mean follow-up of 7.1 years. Following adjustments for demographic and clinical variables, we identified a non-linear relationship between the SRI and all-cause mortality hazard (p [global test of spline term]<0.001). Hazard ratios, relative to the median SRI, were 1.53 (95% confidence interval [CI]: 1.41, 1.66) for participants with SRI at the 5th percentile (SRI = 41) and 0.90 (95% CI: 0.81, 1.00) for those with SRI at the 95th percentile (SRI = 75), respectively. Findings for CVD mortality and cancer mortality followed a similar pattern.

    Conclusions:

    Irregular sleep-wake patterns are associated with higher mortality risk.

    Funding:

    National Health and Medical Research Council of Australia (GTN2009264; GTN1158384), National Institute on Aging (AG062531), Alzheimer’s Association (2018-AARG-591358), and the Banting Fellowship Program (#454104).