Evidence map›Paper›PMID 30598036›Full record

ArticleViruses2018

The Oxysterol 7-Ketocholesterol Reduces Zika Virus Titers in Vero Cells and Human Neurons.

Katherine A Willard, Christina L Elling, Steven L Stice, Melinda A Brindley

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
8.7field-weighted citation impact, top 2% 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

14 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Review
  3. 7-Ketocholesterol: Effects on viral infections and hypothetical contribution in COVID-19.The Journal of steroid biochemistry and molecular biology · 2021
    Review
  4. Review
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  6. Article
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  8. The lysosome: A potential juncture between SARS-CoV-2 infectivity and Niemann-Pick disease type C, with therapeutic implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
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  10. Review
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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

4 authors at 1 institution in 1 country.

Katherine A WillardDepartment of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, USA. katherine.willard@duke.edu.ORCID 0000-0002-0044-2664
Christina L EllingDepartment of Animal and Dairy Science, Regenerative Bioscience Center, College of Agriculture and Environmental Science, University of Georgia, Athens, GA 30602, USA. christina.elling@ucdenver.edu.
Steven L SticeDepartment of Animal and Dairy Science, Regenerative Bioscience Center, College of Agriculture and Environmental Science, University of Georgia, Athens, GA 30602, USA. sstice@uga.edu.
Melinda A BrindleyDepartment of Infectious Diseases, Department of Population Health, Center for Vaccines and Immunology, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, USA. mbrindle@uga.edu.ORCID 0000-0002-4929-8085
University of Georgia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zika virus (ZIKV) is an emerging flavivirus responsible for a major epidemic in the Americas beginning in 2015. ZIKV associated with maternal infection can lead to neurological disorders in newborns, including microcephaly. Although there is an abundance of research examining the neurotropism of ZIKV, we still do not completely understand the mechanism by which ZIKV targets neural cells or how to limit neural cell infection. Recent research suggests that flaviviruses, including ZIKV, may hijack the cellular autophagy pathway to benefit their replication. Therefore, we hypothesized that ZIKV replication would be impacted when infected cells were treated with compounds that target the autophagy pathway. We screened a library of 94 compounds known to affect autophagy in both mammalian and insect cell lines. A subset of compounds that inhibited ZIKV replication without affecting cellular viability were tested for their ability to limit ZIKV replication in human neurons. From this second screen, we identified one compound, 7-ketocholesterol (7-KC), which inhibited ZIKV replication in neurons without significantly affecting neuron viability. Interestingly, 7-KC induces autophagy, which would be hypothesized to increase ZIKV replication, yet it decreased virus production. Time-of-addition experiments suggest 7-KC inhibits ZIKV replication late in the replication cycle. While 7-KC did not inhibit RNA replication, it decreased the number of particles in the supernatant and the relative infectivity of the released particles, suggesting it interferes with particle budding, release from the host cell, and particle integrity.

Indexed as

AnimalsAutophagyCell LineCell SurvivalChlorocebus aethiopsHumansKetocholesterolsNeuronsVero CellsViral LoadVirus InternalizationVirus ReleaseVirus ReplicationZika Virus7-ketocholesterolKetocholesterolsantiviral compoundsneural cellsviral replicationZika virus

Identifiers

PMID30598036
PMCPMC6356585
OpenAlexW2906821738

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.