Evidence map›Paper›PMID 26503654›Full record

ArticleAntimicrobial agents and chemotherapy2016

Modification of the Host Cell Lipid Metabolism Induced by Hypolipidemic Drugs Targeting the Acetyl Coenzyme A Carboxylase Impairs West Nile Virus Replication.

Teresa Merino-Ramos, Ángela Vázquez-Calvo, Josefina Casas, Francisco Sobrino, Juan-Carlos Saiz, Miguel A Martín-Acebes

Open access · greenAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
6.3field-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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 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 3 institutions in 1 country.

Teresa Merino-RamosDepartment of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Madrid, Spain.
Ángela Vázquez-CalvoDepartment of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Madrid, Spain.
Josefina CasasDepartment of Biomedicinal Chemistry, Institute for Advanced Chemistry of Catalonia (IQAC-CSIC), Barcelona, Spain.
Francisco SobrinoDepartment of Virology and Microbiology, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain.
Juan-Carlos SaizDepartment of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Madrid, Spain.
Miguel A Martín-AcebesDepartment of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Madrid, Spain Department of Virology and Microbiology, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain martin.mangel@inia.es.ORCID http://orcid.org/0000-0001-6015-3613
Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria · ESCentro de Biología Molecular Severo Ochoa · ESInstitute of Advanced Chemistry of Catalonia · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

West Nile virus (WNV) is a neurotropic flavivirus transmitted by the bite of mosquitoes that causes meningitis and encephalitis in humans, horses, and birds. Several studies have highlighted that flavivirus infection is highly dependent on cellular lipids for virus replication and infectious particle biogenesis. The first steps of lipid synthesis involve the carboxylation of acetyl coenzyme A (acetyl-CoA) to malonyl-CoA that is catalyzed by the acetyl-CoA carboxylase (ACC). This makes ACC a key enzyme of lipid synthesis that is currently being evaluated as a therapeutic target for different disorders, including cancers, obesity, diabetes, and viral infections. We have analyzed the effect of the ACC inhibitor 5-(tetradecyloxy)-2-furoic acid (TOFA) on infection by WNV. Lipidomic analysis of TOFA-treated cells confirmed that this drug reduced the cellular content of multiple lipids, including those directly implicated in the flavivirus life cycle (glycerophospholipids, sphingolipids, and cholesterol). Treatment with TOFA significantly inhibited the multiplication of WNV in a dose-dependent manner. Further analysis of the antiviral effect of this drug showed that the inhibitory effect was related to a reduction of viral replication. Furthermore, treatment with another ACC inhibitor, 3,3,14,14-tetramethylhexadecanedioic acid (MEDICA 16), also inhibited WNV infection. Interestingly, TOFA and MEDICA 16 also reduced the multiplication of Usutu virus (USUV), a WNV-related flavivirus. These results point to the ACC as a druggable cellular target suitable for antiviral development against WNV and other flaviviruses.

Indexed as

Acetyl-CoA CarboxylaseAnimalsAntiviral AgentsCell LineChlorocebus aethiopsCholesterolEnzyme InhibitorsFuransGene ExpressionGlycerophospholipidsHeLa CellsHost-Pathogen InteractionsHumansHypolipidemic AgentsLipid MetabolismMice5-(tetradecyloxy)-2-furancarboxylic acidAcetyl-CoA CarboxylaseAntiviral AgentsCholesterolEnzyme InhibitorsFuransGlycerophospholipidsHypolipidemic AgentsMEDICA 16Palmitic AcidsSphingolipids

Identifiers

PMID26503654
PMCPMC4704205
OpenAlexW2281439776

What OpenQuestion holds

Textmetadata
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.