Evidence map›Paper›PMID 36016357›Full record

ArticleViruses2022

CD24 Expression Dampens the Basal Antiviral State in Human Neuroblastoma Cells and Enhances Permissivity to Zika Virus Infection.

Kritika Kedarinath, Candace R Fox, Erin Crowgey, Joseph Mazar, Peter Phelan, Tamarah J Westmoreland, Kenneth A Alexander, Griffith D Parks

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Surprising magic of CD24 beyond cancer.Frontiers in immunology · 2023
    Review
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 2 institutions in 1 country.

Kritika KedarinathBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32827, USA.
Candace R FoxBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32827, USA.ORCID 0000-0002-3229-2920
Erin CrowgeyResearch Department, Nemours Children's Hospital Delaware, Wilmington, DE 19803, USA.ORCID 0000-0002-2037-0389
Joseph MazarDepartment of Biomedical Research, Nemours Children's Hospital, Orlando, FL 32827, USA.
Peter PhelanDepartment of Biomedical Research, Nemours Children's Hospital, Orlando, FL 32827, USA.
Tamarah J WestmorelandCollege of Medicine, University of Central Florida, Orlando, FL 32827, USA.
Kenneth A AlexanderCollege of Medicine, University of Central Florida, Orlando, FL 32827, USA.ORCID 0000-0003-3921-5722
Griffith D ParksBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32827, USA.
University of Central Florida · USNemours Children's Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zika virus (ZIKV) exhibits distinct selectivity for infection of various cells and tissues, but how host cellular factors modulate varying permissivity remains largely unknown. Previous studies showed that the neuroblastoma cell line SK-N-AS (expressing low levels of cellular protein CD24) was highly restricted for ZIKV infection, and that this restriction was relieved by ectopic expression of CD24. We tested the hypothesis that CD24 expression allowed ZIKV replication by suppression of the antiviral response. SK-N-AS cells expressing an empty vector (termed CD24-low cells) showed elevated basal levels of phosphorylated STAT1, IRF-1, IKKE, and NFκB. In response to exogenously added type I interferon (IFN-I), CD24-low cells had higher-level induction of antiviral genes and activity against two IFN-I-sensitive viruses (VSV and PIV5-P/V) compared to SK-N-AS cells with ectopic CD24 expression (termed CD24-high cells). Media-transfer experiments showed that the inherent antiviral state of CD24-low cells was not dependent on a secreted factor such as IFN-I. Transcriptomics analysis revealed that CD24 expression decreased expression of genes involved in intracellular antiviral pathways, including IFN-I, NFκB, and Ras. Our findings that CD24 expression in neuroblastoma cells represses intracellular antiviral pathways support the proposal that CD24 may represent a novel biomarker in cancer cells for susceptibility to oncolytic viruses.

Indexed as

Interferon Type INeuroblastomaZika VirusZika Virus InfectionAntiviral AgentsCD24 AntigenHumansAntiviral AgentsCD24 AntigenCD24 protein, humanInterferon Type Iantiviral responsesCD24permissivitytype I interferonzika virus

Identifiers

PMID36016357
PMCPMC9416398
OpenAlexW4292513039

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.