Evidence map›Paper›PMID 31423125›Full record

ArticleEXCLI journal2019

Interferon-inducible protein (IFI) 16 regulates Chikungunya and Zika virus infection in human skin fibroblasts.

Sineewanlaya Wichit, Rodolphe Hamel, Sakda Yainoy, Nuttamonpat Gumpangseth, Suchawadee Panich, Thanawat Phuadraksa, Phoonthawee Saetear, Arnaud Monteil, Ronald Morales Vargas, Dorothée Missé

Open access · greenAbstract read
In one paragraph

Article in EXCLI journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

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  10. Interplay between RNA viruses and cGAS/STING axis in innate immunity.Frontiers in cellular and infection microbiology · 2023
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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

10 authors at 4 institutions in 2 countries.

Sineewanlaya WichitDepartment of Clinical Microbiology and Applied Technology, Faculty of Medical Technology, Mahidol University, Nakhon Pathom, 73170, Thailand.
Rodolphe HamelLaboratoire MIVEGEC, IRD-CNRS-University of Montpellier, 34000, Montpellier, France.
Sakda YainoyDepartment of Clinical Microbiology and Applied Technology, Faculty of Medical Technology, Mahidol University, Nakhon Pathom, 73170, Thailand.
Nuttamonpat GumpangsethDepartment of Clinical Microbiology and Applied Technology, Faculty of Medical Technology, Mahidol University, Nakhon Pathom, 73170, Thailand.
Suchawadee PanichDepartment of Clinical Microbiology and Applied Technology, Faculty of Medical Technology, Mahidol University, Nakhon Pathom, 73170, Thailand.
Thanawat PhuadraksaDepartment of Clinical Microbiology and Applied Technology, Faculty of Medical Technology, Mahidol University, Nakhon Pathom, 73170, Thailand.
Phoonthawee SaetearDepartment of Chemistry and Center of Excellence for Innovation in Chemistry, Faculty of Science, Mahidol University, Bangkok 10400, Thailand.
Arnaud MonteilPlateforme de Vectorologie, BioCampus, Univ. Montpellier, CNRS, INSERM, 34094, Montpellier, France.
Ronald Morales VargasDepartment of Medical Entomology, Faculty of Tropical Medicine, Mahidol University, Bangkok, 10400, Thailand.
Dorothée MisséLaboratoire MIVEGEC, IRD-CNRS-University of Montpellier, 34000, Montpellier, France.
Mahidol University · THCentre National de la Recherche Scientifique · FRInstitut de Recherche pour le Développement · FRMahidol Oxford Tropical Medicine Research Unit · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chikungunya virus (CHIKV), a re-emerging infectious arbovirus, causes Chikungunya fever that is characterized by fever, skin rash, joint pain, arthralgia and occasionally death. Despite it has been described for 66 years already, neither potential vaccine nor a specific drug is available yet. During CHIKV infection, interferon type I signaling pathway is stimulated and releases hundreds of interferon stimulated genes (ISGs). Our previous study reported that IFI16, a member of ISGs, is up-regulated during CHIKV virus infection and the suppression of the gene resulted in increased virus replication. Furthermore, our group also found that inflammasome activation can inhibit CHIKV infection in human foreskin cells (HFF1). Concomitantly, it has been reported that IFI16 activates the inflammasome to suppress virus infection. Therefore, we have hypothesized that IFI16 could be involved in CHIKV infection. In this study, we confirmed the expression level of IFI16 by Western blotting analysis and found that IFI16 was up-regulated following CHIKV infection in both HFF1 and human embryonic kidney cells. We next investigated its antiviral activity and found that forced expression of IFI16 completely restricted CHIKV infection while endogenous silencing of the gene markedly increased virus replication. Furthermore, we have discovered that IFI16 inhibited CHIKV replication, at least, in cell-to-cell transmission as well as the diffusion step. Interestingly, IFI16 also exerted its antiviral activity against Zika virus (ZIKV) infection, the global threat re-emerging virus can cause microcephaly in humans. Taken together, this study provides the first evidence of an antivirus activity of IFI16 during

Indexed as

antiviralChikungunya virushuman skin fibroblastsIFI16Zika virus

Identifiers

PMID31423125
PMCPMC6694701
OpenAlexW2954519661

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.