Evidence map›Paper›PMID 32797077›Full record

ArticlePLoS computational biology2020

Vector genetics, insecticide resistance and gene drives: An agent-based modeling approach to evaluate malaria transmission and elimination.

Prashanth Selvaraj, Edward A Wenger, Daniel Bridenbecker, Nikolai Windbichler, Jonathan R Russell, Jaline Gerardin, Caitlin A Bever, Milen Nikolov

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Gene drives gaining speed.Nature reviews. Genetics · 2022
    Review
  15. Article
  16. 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

8 authors at 4 institutions in 2 countries.

Prashanth SelvarajInstitute for Disease Modeling, Bellevue, Washington, United States of America.ORCID 0000-0001-7565-2300
Edward A WengerInstitute for Disease Modeling, Bellevue, Washington, United States of America.
Daniel BridenbeckerInstitute for Disease Modeling, Bellevue, Washington, United States of America.ORCID 0000-0002-8200-1706
Nikolai WindbichlerDepartment of Life Sciences, Imperial College London, South Kensington, United Kingdom.ORCID 0000-0001-9896-1165
Jonathan R RussellInstitute for Disease Modeling, Bellevue, Washington, United States of America.ORCID 0000-0002-8295-1621
Jaline GerardinInstitute for Disease Modeling, Bellevue, Washington, United States of America.ORCID 0000-0001-8071-9928
Caitlin A BeverInstitute for Disease Modeling, Bellevue, Washington, United States of America.
Milen NikolovInstitute for Disease Modeling, Bellevue, Washington, United States of America.ORCID 0000-0003-2647-3255
Bellevue Hospital Center · USImperial College London · GBNorthwestern University · USSage Bionetworks · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vector control has been a key component in the fight against malaria for decades, and chemical insecticides are critical to the success of vector control programs worldwide. However, increasing resistance to insecticides threatens to undermine these efforts. Understanding the evolution and propagation of resistance is thus imperative to mitigating loss of intervention effectiveness. Additionally, accelerated research and development of new tools that can be deployed alongside existing vector control strategies is key to eradicating malaria in the near future. Methods such as gene drives that aim to genetically modify large mosquito populations in the wild to either render them refractory to malaria or impair their reproduction may prove invaluable tools. Mathematical models of gene flow in populations, which is the transfer of genetic information from one population to another through migration, can offer invaluable insight into the behavior and potential impact of gene drives as well as the spread of insecticide resistance in the wild. Here, we present the first multi-locus, agent-based model of vector genetics that accounts for mutations and a many-to-many mapping cardinality of genotypes to phenotypes to investigate gene flow, and the propagation of gene drives in Anopheline populations. This model is embedded within a large scale individual-based model of malaria transmission representative of a high burden, high transmission setting characteristic of the Sahel. Results are presented for the selection of insecticide-resistant vectors and the spread of resistance through repeated deployment of insecticide treated nets (ITNs), in addition to scenarios where gene drives act in concert with existing vector control tools such as ITNs. The roles of seasonality, spatial distribution of vector habitat and feed sites, and existing vector control in propagating alleles that confer phenotypic traits via gene drives that result in reduced transmission are explored. The ability to model a spectrum of vector species with different genotypes and phenotypes in the context of malaria transmission allows us to test deployment strategies for existing interventions that reduce the deleterious effects of resistance and allows exploration of the impact of new tools being proposed or developed.

Indexed as

MalariaAnimalsAnophelesGene Drive TechnologyGenetic FitnessHumansInsecticide ResistanceMosquito VectorsSystems Analysis

Identifiers

PMID32797077
PMCPMC7449459
OpenAlexW3049433551

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.