Cited by 796Influenza Virus Research StudiesMathematical and Theoretical Epidemiology and Ecology ModelsViral Infections and Outbreaks Research

Transmissibility of 1918 pandemic influenza

Open access
Mills, Christina E., Robins, James M., Lipsitch, Marc·2004·Nature

Abstract

The 1918 influenza pandemic killed 20-40 million people worldwide, and is seen as a worst-case scenario for pandemic planning. Like other pandemic influenza strains, the 1918 A/H1N1 strain spread extremely rapidly. A measure of transmissibility and of the stringency of control measures required to stop an epidemic is the reproductive number, which is the number of secondary cases produced by each primary case. Here we obtained an estimate of the reproductive number for 1918 influenza by fitting a deterministic SEIR (susceptible-exposed-infectious-recovered) model to pneumonia and influenza death epidemic curves from 45 US cities: the median value is less than three. The estimated proportion of the population with A/H1N1 immunity before September 1918 implies a median basic reproductive number of less than four. These results strongly suggest that the reproductive number for 1918 pandemic influenza is not large relative to many other infectious diseases. In theory, a similar novel influenza subtype could be controlled. But because influenza is frequently transmitted before a specific diagnosis is possible and there is a dearth of global antiviral and vaccine stores, aggressive transmission reducing measures will probably be required.

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  • Sensitivity analyses considered lags of 7 or 10 days in calculating the CEPID to account for the interval between infection and death.

    “In sensitivity analyses performed to account for the interval between infection (the true measure of transmission) and death (an outcome of infection), we also considered lags of 7 or 10 days in calculating the CEPID”

    From Public health interventions and epidemic intensity during the 1918 influenza pandemic (2007) · cites this paper as [12]

    The Main section models a delay between infection and death and reports sensitivity analyses of the time-to-death distribution. It does not mention CEPID or calculating it with lags of 7 or 10 days; those appear to be the citing authors’ own choices. (LLM, conf=0.86)

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Research works printed but not linked: 1

  1. [23]Olson DR Simonsen L Edelson PJ Morse SS 4th Int. Conf. on Emerging Infectious Diseases 2004

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Authors
Mills, C. E., Robins, J. M., & Lipsitch, M.
Affiliations
Harvard University (US)
Corresponding author
Mills, Christina E.
Venue
Nature
Published
2004-12
Volume
432
Issue
7019
Pages
904-906
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
OpenAlex
W2037844075
Cited by
796
References
44
Citations by year
2026: 9 · 2025: 12 · 2024: 19 · 2023: 28 · 2022: 38 · 2021: 47 · 2020: 84 · 2019: 20 · 2018: 22 · 2017: 21 · 2016: 21 · 2015: 29 · 2014: 40 · 2013: 39 · 2012: 36
FWCI
28.36
Type
journal article
Language
en
Open access
Locations
  • Nature (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
Funders
  • U.S. Department of Health and Human Services
  • Ellison Medical Foundation
  • National Defense Science and Engineering Graduate
  • National Institute of Allergy and Infectious Diseases
  • Fogarty International Center
Topics
  • Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Mathematical and Theoretical Epidemiology and Ecology Models
  • Health Sciences › Medicine › Infectious Diseases › Viral Infections and Outbreaks Research
Keywords
1918 influenza pandemic, H1N1 influenza, basic reproduction number, transmissibility, SEIR model, epidemic curve, pandemic preparedness
MeSH terms
Cities, Communicable Disease Control, Humans, Influenza, Human, Models, Biological, Probability, Time Factors, United States, Survival Analysis, History, 20th Century

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