Evidence map›Paper›PMID 33097713›Full record

ArticleNature communications2020

Increased power from conditional bacterial genome-wide association identifies macrolide resistance mutations in Neisseria gonorrhoeae.

Kevin C Ma, Tatum D Mortimer, Marissa A Duckett, Allison L Hicks, Nicole E Wheeler, Leonor Sánchez-Busó, Yonatan H Grad

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 64 citations in OpenAlex.

  1. Heterogeneity of azithromycin resistance markers inNew microbes and new infections · 2026
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  11. CommensalAnnual review of microbiology · 2025
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  19. Rolling the evolutionary dice:Microbiology spectrum · 2024
    Article
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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 at 3 institutions in 2 countries.

Kevin C MaDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.ORCID 0000-0002-4326-2911
Tatum D MortimerDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.ORCID 0000-0001-6255-690X
Marissa A DuckettDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Allison L HicksDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.ORCID 0000-0003-1372-1301
Nicole E WheelerCentre for Genomic Pathogen Surveillance, Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK.ORCID 0000-0003-4599-9164
Leonor Sánchez-BusóCentre for Genomic Pathogen Surveillance, Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, UK.ORCID 0000-0002-4162-0228
Yonatan H GradDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA. ygrad@hsph.harvard.edu.ORCID 0000-0001-5646-1314
Harvard University · USWellcome Sanger Institute · GBBrigham and Women's Hospital · US

Funding

Genomics approaches to elucidating pathways to antibiotic resistance in Neisseria gonorrhoeaeR01AI132606 · NIAID · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI Yonatan H Grad · 2017 to 2026
$3.8M
Acquisition, maintenance, and transmission of antibiotic resistance in Neisseria gonorrhoeaeF32AI145157 · NIAID · HARVARD SCHOOL OF PUBLIC HEALTH · PI MORTIMER, TATUM DANIELLE · 2019 to 2021
$200k
NIAID NIH HHS F32 AI145157NIAID NIH HHS R01 AI132606
6 · The paper itself

Abstract

The emergence of resistance to azithromycin complicates treatment of Neisseria gonorrhoeae, the etiologic agent of gonorrhea. Substantial azithromycin resistance remains unexplained after accounting for known resistance mutations. Bacterial genome-wide association studies (GWAS) can identify novel resistance genes but must control for genetic confounders while maintaining power. Here, we show that compared to single-locus GWAS, conducting GWAS conditioned on known resistance mutations reduces the number of false positives and identifies a G70D mutation in the RplD 50S ribosomal protein L4 as significantly associated with increased azithromycin resistance (p-value = 1.08 × 10

Indexed as

Genome, BacterialGenome-Wide Association StudyAnti-Bacterial AgentsAzithromycinBinding SitesDrug Resistance, BacterialGonorrheaHumansMacrolidesMicrobial Sensitivity TestsMutationNeisseria gonorrhoeaeRNA, Ribosomal, 23SAnti-Bacterial AgentsAzithromycinMacrolidesRNA, Ribosomal, 23S

Identifiers

PMID33097713
PMCPMC7584619
OpenAlexW3093665745

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.