Evidence map›Paper›PMID 32493846›Full record

ArticleJCI insight2020

Streptococcus pyogenes genes that promote pharyngitis in primates.

Luchang Zhu, Randall J Olsen, Stephen B Beres, Matthew Ojeda Saavedra, Samantha L Kubiak, Concepcion C Cantu, Leslie Jenkins, Andrew S Waller, Zhizeng Sun, Timothy Palzkill and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Trial
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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

13 authors at 4 institutions in 2 countries.

Luchang ZhuCenter for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas, USA.
Randall J OlsenCenter for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas, USA.
Stephen B BeresCenter for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas, USA.
Matthew Ojeda SaavedraCenter for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas, USA.
Samantha L KubiakCenter for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas, USA.
Concepcion C CantuCenter for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas, USA.
Leslie JenkinsDepartment of Comparative Medicine, Houston Methodist Research Institute, Houston, Texas, USA.
Andrew S WallerAnimal Health Trust, Lanwades Park, Newmarket, United Kingdom.
Zhizeng SunDepartment of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, Texas, USA.
Timothy PalzkillDepartment of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, Texas, USA.
Adeline R PorterLaboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, NIH, Hamilton, Montana, USA.
Frank R DeLeoLaboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, NIH, Hamilton, Montana, USA.
James M MusserCenter for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, and Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas, USA.
Houston Methodist · USBaylor College of Medicine · USNational Institute of Allergy and Infectious Diseases · USAnimal Health Trust · GB

Funding

BETA-LACTAMASE MUTATIONS IN ANTIBIOTIC RESISTANCER01AI032956 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI Timothy Palzkill · 1992 to 2026
$6.5M
Interaction of pathogenic bacteria with human phagocytic leukocytesZIAAI000900 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DELEO, FRANK · 2009 to 2023
$3.6M
Beta Lactamase Mutations in Antibiotic ResistanceR37AI032956 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI PALZKILL, TIMOTHY · 2001 to 2010
$3.3M
Determinants of Streptococcus pyogenes virulence in the primate oropharynx: A genome-wide analysisR21AI139369 · NIAID · METHODIST HOSPITAL RESEARCH INSTITUTE · PI MUSSER, JAMES MALLORY · 2019 to 2020
$444k
Determinants of Streptococcus pyogenes fitness in the female primate genital tract: A genome-wide analysisR21AI146771 · NIAID · METHODIST HOSPITAL RESEARCH INSTITUTE · PI MUSSER, JAMES MALLORY · 2019 to 2020
$444k
Beta Lactamase Mutations in Antibiotic ResistanceR56AI032956 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI PALZKILL, TIMOTHY · 2016 to 2016
$394k
NIAID NIH HHS R01 AI032956NIAID NIH HHS R21 AI139369NIAID NIH HHS R21 AI146771NIAID NIH HHS R37 AI032956NIAID NIH HHS R56 AI032956
6 · The paper itself

Abstract

Streptococcus pyogenes (group A streptococcus; GAS) causes 600 million cases of pharyngitis annually worldwide. There is no licensed human GAS vaccine despite a century of research. Although the human oropharynx is the primary site of GAS infection, the pathogenic genes and molecular processes used to colonize, cause disease, and persist in the upper respiratory tract are poorly understood. Using dense transposon mutant libraries made with serotype M1 and M28 GAS strains and transposon-directed insertion sequencing, we performed genome-wide screens in the nonhuman primate (NHP) oropharynx. We identified many potentially novel GAS fitness genes, including a common set of 115 genes that contribute to fitness in both genetically distinct GAS strains during experimental NHP pharyngitis. Targeted deletion of 4 identified fitness genes/operons confirmed that our newly identified targets are critical for GAS virulence during experimental pharyngitis. Our screens discovered many surface-exposed or secreted proteins - substrates for vaccine research - that potentially contribute to GAS pharyngitis, including lipoprotein HitA. Pooled human immune globulin reacted with purified HitA, suggesting that humans produce antibodies against this lipoprotein. Our findings provide new information about GAS fitness in the upper respiratory tract that may assist in translational research, including developing novel vaccines.

Indexed as

Genes, BacterialPharyngitisStreptococcal InfectionsStreptococcus pyogenesVirulence FactorsAnimalsDisease Models, AnimalGenome-Wide Association StudyHumansMacaca fascicularisVirulence FactorsBacterial infectionsInfectious disease

Identifiers

PMID32493846
PMCPMC7308061
OpenAlexW3031044782

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.