Evidence map›Paper›PMID 12196403›Full record

ArticleGenetics2002

Historical intensity of natural selection for resistance to tuberculosis.

Marc Lipsitch, Alexandra O Sousa

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 52 citations in OpenAlex.

  1. Gaucher disease protects against tuberculosis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  2. Genetic Resistance toFrontiers in immunology · 2018
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Non-clinical factors associated with TB: important for DOTS impact evaluation and disease elimination.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2014
    Article
  10. Article
  11. Old and new selective pressures on Mycobacterium tuberculosis.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2012
    Review
  12. Host-pathogen coevolution in human tuberculosis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2012
    Review
  13. Article
  14. Review
  15. Article
  16. Article
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  19. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Marc LipsitchDepartments of Epidemiology, Harvard School of Public Health, Boston, Massachusetts 02115, USA. mlipsitc@hsph.harvard.edu
Alexandra O Sousa
Harvard University · USRockefeller University · US

Funding

VACCINATION AND THE EVOLUTIONARY DYNAMICS OF PNEUMOCOCCIR01AI048935 · NIAID · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI LIPSITCH, MARC · 2001 to 2016
$8.8M
NIAID NIH HHS R01 AI48935
6 · The paper itself

Abstract

Infections have long been thought to exert natural selection on humans. Infectious disease resistance is frequently invoked as a mechanism shaping human genetic diversity, but such hypotheses have rarely been quantitatively evaluated with direct measures of disease-related mortality. Enhancement of genetically determined resistance to tuberculosis by natural selection has been proposed as a factor explaining the decline of tuberculosis in Europe and North America in the period 1830-1950 (before the advent of antimicrobial chemotherapy) and the apparently reduced susceptibility of Europeans and their descendants to tuberculosis infection and/or disease. We used Swedish vital statistics from 1891 to 1900 to estimate that individuals who escaped mortality from pulmonary tuberculosis (PTB) during the European tuberculosis epidemic would have enjoyed a fitness advantage of 7-15% per generation compared to individuals who were susceptible to PTB mortality; individuals with 50% protection would have had a selection coefficient of 4-7%/generation. Selection during the peak of the European TB epidemic could have substantially reduced the frequency of already rare alleles conferring increased susceptibility to PTB mortality, but only if the phenotypic effects of these alleles were very large. However, if resistant alleles were rare at the beginning of this period, 300 years would not have been long enough for such selection to increase their frequency to epidemiologically significant levels. Reductions in the frequency of rare susceptibility alleles could have played at most a small part in the decline of the epidemic in the century preceding 1950. Natural selection by PTB deaths during the European TB epidemic alone cannot account for the presently low level of TB disease observed among Europeans and their descendants just prior to the appearance of antibiotic treatment.

Indexed as

Selection, GeneticFemaleHumansImmunity, InnateMaleMortalityTuberculosis

Identifiers

PMID12196403
PMCPMC1462208
OpenAlexW1834942435

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.