Evidence map›Paper›PMID 35634338›Full record

ArticleFrontiers in immunology2022

Time-Dependent Increase in Susceptibility and Severity of Secondary Bacterial Infections During SARS-CoV-2.

Amanda P Smith, Evan P Williams, Taylor R Plunkett, Muneeswaran Selvaraj, Lindey C Lane, Lillian Zalduondo, Yi Xue, Peter Vogel, Rudragouda Channappanavar, Colleen B Jonsson and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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  5. Post-pandemic upsurge in Group AMicrobiology spectrum · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Amanda P SmithDepartment of Pediatrics, University of Tennessee Health Science Center, Memphis, TN, United States.
Evan P WilliamsDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
Taylor R PlunkettDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
Muneeswaran SelvarajDepartment of Acute and Tertiary Care, University of Tennessee Health Science Center, Memphis, TN, United States.
Lindey C LaneCollege of Pharmacy, University of Tennessee Health Science Center, Memphis, TN, United States.
Lillian ZalduondoDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
Yi XueDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
Peter VogelAnimal Resources Center and Veterinary Pathology Core, St. Jude Children's Research Hospital, Memphis, TN, United States.
Rudragouda ChannappanavarDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
Colleen B JonssonDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States.
Amber M SmithDepartment of Pediatrics, University of Tennessee Health Science Center, Memphis, TN, United States.
University of Tennessee Health Science Center · USSt. Jude Children's Research Hospital · US

Funding

Predictive Modeling of Influenza-Pneumococcal CoinfectionR01AI139088 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SMITH, AMBER M · 2018 to 2022
$2.1M
NIAID NIH HHS R01 AI139088
6 · The paper itself

Abstract

Secondary bacterial infections can exacerbate SARS-CoV-2 infection, but their prevalence and impact remain poorly understood. Here, we established that a mild to moderate infection with the SARS-CoV-2 USA-WA1/2020 strain increased the risk of pneumococcal (type 2 strain D39) coinfection in a time-dependent, but sex-independent, manner in the transgenic K18-hACE2 mouse model of COVID-19. Bacterial coinfection increased lethality when the bacteria was initiated at 5 or 7 d post-virus infection (pvi) but not at 3 d pvi. Bacterial outgrowth was accompanied by neutrophilia in the groups coinfected at 7 d pvi and reductions in B cells, T cells, IL-6, IL-15, IL-18, and LIF were present in groups coinfected at 5 d pvi. However, viral burden, lung pathology, cytokines, chemokines, and immune cell activation were largely unchanged after bacterial coinfection. Examining surviving animals more than a week after infection resolution suggested that immune cell activation remained high and was exacerbated in the lungs of coinfected animals compared with SARS-CoV-2 infection alone. These data suggest that SARS-CoV-2 increases susceptibility and pathogenicity to bacterial coinfection, and further studies are needed to understand and combat disease associated with bacterial pneumonia in COVID-19 patients.

Indexed as

Bacterial InfectionsCoinfectionCOVID-19AnimalsBacteriaHumansMiceMice, TransgenicSARS-CoV-2coinfectionCOVID-19immune responsepneumococcusSARS-CoV-2Streptococcus pnemoniae

Identifiers

PMID35634338
PMCPMC9134015
OpenAlexW4280560189

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.