Evidence map›Paper›PMID 32194565›Full record

ArticleFrontiers in immunology2020

HSV-2 Infection of Human Genital Epithelial Cells Upregulates TLR9 Expression Through the SP1/JNK Signaling Pathway.

Kai Hu, Ming Fu, Jun Wang, Sukun Luo, Mariana Barreto, Rubin Singh, Tasnim Chowdhury, Mei Li, Mudan Zhang, Xinmeng Guan and 2 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2020. 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
–field-weighted citation impact
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.

  1. Review
  2. Review
  3. Beyond the Barrier: Epithelial Cells as Immune Sentinels in the Female Genital Tract.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    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

12 authors.

Kai HuInstitute for Infection and Immunity, St George's, University of London, London, United Kingdom.
Ming FuState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Jun WangInstitute for Clinical Research Center, Wuhan Medical and Healthcare Center for Women and Children, Wuhan, China.
Sukun LuoInstitute for Clinical Research Center, Wuhan Medical and Healthcare Center for Women and Children, Wuhan, China.
Mariana BarretoInstitute for Infection and Immunity, St George's, University of London, London, United Kingdom.
Rubin SinghInstitute for Infection and Immunity, St George's, University of London, London, United Kingdom.
Tasnim ChowdhuryInstitute for Infection and Immunity, St George's, University of London, London, United Kingdom.
Mei LiState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Mudan ZhangState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Xinmeng GuanInstitute for Infection and Immunity, St George's, University of London, London, United Kingdom.
Juhua XiaoDepartment of Ultrasound, Jiangxi Provincial Maternal and Child Health Hospital, Nanchang, China.
Qinxue HuInstitute for Infection and Immunity, St George's, University of London, London, United Kingdom.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is known that herpes simplex virus type 2 (HSV-2) triggers the activation of Toll-like receptor (TLR) 9 signaling pathway and the consequent production of antiviral cytokines in dendritic cells. However, the impact of HSV-2 infection on TLR9 expression and signaling in genital epithelial cells, the primary HSV-2 targets, has yet to be determined. In the current study, by using both human genital epithelial cell lines and primary genital epithelial cells as models, we found that HSV-2 infection enhances TLR9 expression at both mRNA and protein levels. Such enhancement is virus replication-dependent and CpG-independent, while the HSV-2-mediated upregulation of TLR9 does not activate TLR9 signaling pathway. Mechanistically, a SP1 binding site on TLR9 promoter appears to be essential for HSV-2-induced TLR9 transactivation. Upon HSV-2 infection, SP1 translocates from the cytoplasm to the nucleus, and consequently binds to TLR9 promoter. By using specific inhibitors, the JNK signaling pathway is shown to be involved in the HSV-2-induced TLR9 transactivation, while HSV-2 infection increases the phosphorylation but not the total level of JNK. In agreement, antagonism of JNK signaling pathway inhibits the HSV-2-induced SP1 nuclear translocation. Taken together, our study demonstrates that HSV-2 infection of human genital epithelial cells promotes TLR9 expression through SP1/JNK signaling pathway. Findings in this study provide insights into HSV-2-host interactions and potential targets for immune intervention.

Indexed as

Epithelial CellsFemaleGenitaliaHeLa CellsHerpesvirus 2, HumanHumansJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Signaling SystemPromoter Regions, GeneticSignal TransductionSp1 Transcription FactorToll-Like Receptor 9Up-RegulationVirus ReplicationJNK Mitogen-Activated Protein KinasesSP1 protein, humanSp1 Transcription FactorTLR9 protein, humanToll-Like Receptor 9genital epithelial cellsherpes simplex virus type 2JNK pathwayspecificity protein 1toll-like receptor 9

Identifiers

PMID32194565
PMCPMC7065266

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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.