Evidence map›Paper›PMID 36209057›Full record

ArticleBMC genomics2022

Revealing the characteristics of ZIKV infection through tissue-specific transcriptome sequencing analysis.

Zhi-Lu Chen, Zuo-Jing Yin, Tian-Yi Qiu, Jian Chen, Jian Liu, Xiao-Yan Zhang, Jian-Qing Xu

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.8field-weighted citation impact, top 15% 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, 10 citations in OpenAlex.

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  5. Review
  6. Unraveling flavivirus pathogenesis: from bulk to single-cell RNA-sequencing strategies.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    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

7 authors at 2 institutions in 1 country.

Zhi-Lu Chen *Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Zuo-Jing Yin *Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Tian-Yi Qiu *Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China. ty_qiu@126.com.
Jian ChenShanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.
Jian LiuShanghai Public Health Clinical Center, Fudan University, Shanghai, 201508, China.
Xiao-Yan ZhangInstitutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China. zhangxiaoyan@fudan.edu.cn.
Jian-Qing XuInstitutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China. xujianqing@fudan.edu.cn.
Shanghai Medical College of Fudan University · CNShanghai Public Health Clinical Center · CN

Funding

National Natural Science Foundation of China 31900483National Natural Science Foundation of China 81901598National Natural Science Foundation of China 82071788
6 · The paper itself

Abstract

backgroundRecently, Zika virus (ZIKV) re-emerged in India and was potentially associated with microcephaly. However, the molecular mechanisms underlying ZIKV pathogenesis remain to be explored.

resultsHerein, we performed a comprehensive RNA-sequencing analysis on ZIKV-infected JEG-3, U-251 MG, and HK-2 cells versus corresponding uninfected controls. Combined with a series of functional analyses, including gene annotation, pathway enrichment, and protein-protein interaction (PPI) network analysis, we defined the molecular characteristics induced by ZIKV infection in different tissues and invasion time points. Data showed that ZIKV infection and replication in each susceptible organ commonly stimulated interferon production and down-regulated metabolic-related processes. Also, tissue-specific immune responses or biological processes (BPs) were induced after ZIKV infection, including GnRH signaling pathway in JEG-3 cells, MAPK signaling pathway in U-251 MG cells, and PPAR signaling pathway in HK-2 cells. Of note, ZIKV infection induced delayed antiviral interferon responses in the placenta-derived cell lines, which potentially explains the molecular mechanism by which ZIKV replicates rapidly in the placenta and subsequential vertical transmission occurs.

conclusionsTogether, these data may provide a systemic insight into the pathogenesis of ZIKV infection in distinct human tissue-derived cell lines, which is likely to help develop prophylactic and therapeutic strategies against ZIKV infection.

Indexed as

Zika VirusZika Virus InfectionAntiviral AgentsCell Line, TumorGonadotropin-Releasing HormoneHumansInterferonsPeroxisome Proliferator-Activated ReceptorsRNATranscriptomeVirus ReplicationAntiviral AgentsGonadotropin-Releasing HormoneInterferonsPeroxisome Proliferator-Activated ReceptorsRNAHost immune responsesTissue-specificTranscriptome sequencing analysisType I interferonZika virus

Identifiers

PMID36209057
PMCPMC9546753
OpenAlexW4303613993

What OpenQuestion holds

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LicenceCC BY
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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.