Evidence map›Paper›PMID 28442752›Full record

ArticleEmerging microbes & infections2017

Zika virus infection reprograms global transcription of host cells to allow sustained infection.

Shashi Kant Tiwari, Jason Dang, Yue Qin, Gianluigi Lichinchi, Vikas Bansal, Tariq M Rana

Open access · goldAbstract read
In one paragraph

Article in Emerging microbes & infections, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing 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

51 citing papers in PubMed, 71 citations in OpenAlex.

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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

6 authors at 1 institution in 2 countries.

Shashi Kant TiwariDepartment of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
Jason DangDepartment of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
Yue QinDepartment of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
Gianluigi LichinchiDepartment of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
Vikas BansalDepartment of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
Tariq M RanaDepartment of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA.
University of San Diego · US

Funding

Mechanisms of innate immunity against HIVR01AI043198 · NIAID · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI RANA, TARIQ M · 1998 to 2014
$4.7M
Modeling HIV/AIDS Associated Neurological Disorders with Human Pluripotent CellsDP1DA039562 · NIDA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RANA, TARIQ M · 2015 to 2020
$3.9M
Regulation of HIV-1 Replication by Cellular IncRNAsR21AI125103 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RANA, TARIQ M · 2016 to 2017
$426k
NIAID NIH HHS R01 AI043198NIAID NIH HHS R21 AI125103NIDA NIH HHS DP1 DA039562
6 · The paper itself

Abstract

Zika virus (ZIKV) is an emerging virus causally linked to neurological disorders, including congenital microcephaly and Guillain-Barré syndrome. There are currently no targeted therapies for ZIKV infection. To identify novel antiviral targets and to elucidate the mechanisms by which ZIKV exploits the host cell machinery to support sustained replication, we analyzed the transcriptomic landscape of human microglia, fibroblast, embryonic kidney and monocyte-derived macrophage cell lines before and after ZIKV infection. The four cell types differed in their susceptibility to ZIKV infection, consistent with differences in their expression of viral response genes before infection. Clustering and network analyses of genes differentially expressed after ZIKV infection revealed changes related to the adaptive immune system, angiogenesis and host metabolic processes that are conducive to sustained viral production. Genes related to the adaptive immune response were downregulated in microglia cells, suggesting that ZIKV effectively evades the immune response after reaching the central nervous system. Like other viruses, ZIKV diverts host cell resources and reprograms the metabolic machinery to support RNA metabolism, ATP production and glycolysis. Consistent with these transcriptomic analyses, nucleoside metabolic inhibitors abrogated ZIKV replication in microglia cells.

Indexed as

Adaptive ImmunityAdenosine TriphosphateAnimalsAntiviral AgentsCell Line, TumorChlorocebus aethiopsFibroblastsFloxuridineFluorouracilGene Expression ProfilingGlycolysisHEK293 CellsHost-Pathogen InteractionsHumansKidneyMacrophagesAdenosine TriphosphateAntiviral AgentsFloxuridineFluorouracilRNA

Identifiers

PMID28442752
PMCPMC5457678
OpenAlexW2609139828

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.