Evidence map›Paper›PMID 26411318›Full record

ArticleVirology journal2015

Interferon lambda inhibits dengue virus replication in epithelial cells.

Helen K Palma-Ocampo, Juan C Flores-Alonso, Verónica Vallejo-Ruiz, Julio Reyes-Leyva, Lilian Flores-Mendoza, Irma Herrera-Camacho, Nora H Rosas-Murrieta, Gerardo Santos-López

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 65 citations in OpenAlex.

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  11. Exposing the Two Contrasting Faces of STAT2 in Inflammation.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022
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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

8 authors at 2 institutions in 1 country.

Helen K Palma-OcampoLaboratorio de Biología Molecular y Virología, Centro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Metepec, Puebla, México. hk.palma@gmail.com.
Juan C Flores-AlonsoLaboratorio de Biología Molecular y Virología, Centro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Metepec, Puebla, México. flores_alonso_jc@hotmail.com.
Verónica Vallejo-RuizLaboratorio de Biología Molecular y Virología, Centro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Metepec, Puebla, México. veronica_vallejo@yahoo.com.
Julio Reyes-LeyvaLaboratorio de Biología Molecular y Virología, Centro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Metepec, Puebla, México. julio.reyes@imss.gob.mx.
Lilian Flores-MendozaLaboratorio de Inmunología, Centro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla, México. liliankarem@gmail.com.
Irma Herrera-CamachoLaboratorio de Bioquímica, Centro de Química, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla, Puebla, México. irma.herrera@correo.buap.mx.
Nora H Rosas-MurrietaLaboratorio de Bioquímica, Centro de Química, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla, Puebla, México. nora.rosas@correo.buap.mx.
Gerardo Santos-LópezLaboratorio de Biología Molecular y Virología, Centro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Metepec, Puebla, México. gerardo.santos.lopez@gmail.com.
Mexican Social Security Institute · MXBenemérita Universidad Autónoma de Puebla · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn viral disease, infection is controlled at the cellular level by type I interferon (IFN-I), but dengue virus (DENV) has the ability to inhibit this response. Type III interferon, also known as lambda IFN (IFN-III or IFN-λ), is a complementary pathway to the antiviral response by IFN-I. This work analyzed the IFN-λ (IFN-III) mediated antiviral response against DENV serotype 2 (DENV-2) infection.

methodsDengue fever patients were sampled to determine their IFN-λ levels by ELISA. To study the IFN-λ response during DENV infection we selected the epithelial cell line C33-A, and we demonstrated that it is permissive to DENV-2 infection. The effect of IFN-λ on virus replication was determined in these cells, in parallel to the expression of IFN-stimulated genes (ISGs), and Suppressor of Cytokine Signaling (SOCS), genes measured by RT-qPCR.

resultsWe found increased (~1.8 times) serological IFN-λ in dengue fever patients compared to healthy blood donors. IFN-λ inhibited DENV-2 replication in a dose-dependent manner in vitro. The reduction of viral titer corresponded with increased ISG mRNA levels (MX1 and OAS1), with the highest inhibition occurring at ISG's peak expression. Presence of IFN-negative regulators, SOCS1 and SOCS3, during DENV-2 infection was associated with reduced IFN-λ1 expression.

conclusionsEvidence described here suggests that IFN-λ is a good candidate inhibitor of viral replication in dengue infection. Mechanisms for the cellular and organismal interplay between DENV and IFN- λ need to be further studied as they could provide insights into strategies to treat this disease. Furthermore, we report a novel epithelial model to study dengue infection in vitro.

Indexed as

2',5'-Oligoadenylate SynthetaseAntiviral AgentsDengue VirusEpithelial CellsGene Expression ProfilingHumansInterferon LambdaInterferonsInterleukinsMyxovirus Resistance ProteinsRNA, MessengerViral LoadVirus Replication2',5'-Oligoadenylate SynthetaseAntiviral AgentsInterferon Lambdainterferon-lambda, humanInterferonsInterleukinsMX1 protein, humanMyxovirus Resistance ProteinsOAS1 protein, humanRNA, Messenger

Identifiers

PMID26411318
PMCPMC4584467
OpenAlexW2138061944

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.