Evidence map›Paper›PMID 37289806›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

Spreading processes with mutations over multilayer networks.

Mansi Sood, Anirudh Sridhar, Rashad Eletreby, Chai Wah Wu, Simon A Levin, Osman Yağan, H Vincent Poor

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Integrated framework to study genomic surveillance of selective sweeps in multivariants dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Article
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

7 authors.

Mansi SoodDepartment of Electrical and Computer Engineering, Carnegie Mellon University, Pittsburgh, PA 15213.
Anirudh SridharDepartment of Electrical Engineering, Princeton University, Princeton, NJ 08544.
Rashad EletrebyRocket Travel, Inc., Chicago, IL 60661.
Chai Wah WuThomas J. Watson Research Center, IBM, Yorktown Heights, NY 10598.ORCID 0000-0002-0657-0683
Simon A LevinDepartment of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ 08544.ORCID 0000-0002-8216-5639
Osman YağanDepartment of Electrical and Computer Engineering, Carnegie Mellon University, Pittsburgh, PA 15213.
H Vincent PoorDepartment of Electrical Engineering, Princeton University, Princeton, NJ 08544.ORCID 0000-0002-2062-131X

Funding

Carnegie Mellon University (CMU) Cylab Presidential FellowshipDOD | USA | CCDC | Army Research Office (ARO) W911NF-18-1-0325DOD | USA | CCDC | Army Research Office (ARO) W911NF-20-1-0204DOD | USA | CCDC | Army Research Office (ARO) W911NF-22-1-0181Dowd Fellowship N/AGoogle (Google LLC) N/AInternational Business Machines Corporation (IBM) N/AKnight Fellowship N/ALee-Stanziale Ohana Endowed Fellowship N/ANational Science Foundation (NSF) 1813637National Science Foundation (NSF) 1917819National Science Foundation (NSF) 2026985National Science Foundation (NSF) 2041952National Science Foundation (NSF) 2142997National Science Foundation (NSF) 2225513
6 · The paper itself

Abstract

A key scientific challenge during the outbreak of novel infectious diseases is to predict how the course of the epidemic changes under countermeasures that limit interaction in the population. Most epidemiological models do not consider the role of mutations and heterogeneity in the type of contact events. However, pathogens have the capacity to mutate in response to changing environments, especially caused by the increase in population immunity to existing strains, and the emergence of new pathogen strains poses a continued threat to public health. Further, in the light of differing transmission risks in different congregate settings (e.g., schools and offices), different mitigation strategies may need to be adopted to control the spread of infection. We analyze a multilayer multistrain model by simultaneously accounting for i) pathways for mutations in the pathogen leading to the emergence of new pathogen strains, and ii) differing transmission risks in different settings, modeled as network layers. Assuming complete cross-immunity among strains, namely, recovery from any infection prevents infection with any other (an assumption that will need to be relaxed to deal with COVID-19 or influenza), we derive the key epidemiological parameters for the multilayer multistrain framework. We demonstrate that reductions to existing models that discount heterogeneity in either the strain or the network layers may lead to incorrect predictions. Our results highlight that the impact of imposing/lifting mitigation measures concerning different contact network layers (e.g., school closures or work-from-home policies) should be evaluated in connection with their effect on the likelihood of the emergence of new strains.

Indexed as

COVID-19EpidemicsInfluenza, HumanDisease OutbreaksHumansMutationagent-based modelsbranching processesmultilayer networksmutationsnetwork epidemics

Identifiers

PMID37289806
PMCPMC10268263

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.