Evidence map›Paper›PMID 26764042›Full record

ArticleJournal of lipid research2016

Host sphingomyelin increases West Nile virus infection in vivo.

Miguel A Martín-Acebes, Enrique Gabandé-Rodríguez, Ana M García-Cabrero, Marina P Sánchez, María Dolores Ledesma, Francisco Sobrino, Juan-Carlos Saiz

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
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  4. Measles virus reprograms CD4Frontiers in cell and developmental biology · 2026
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  7. Article
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  9. The Implication of Sphingolipids in Viral Infections.International journal of molecular sciences · 2023
    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 4 institutions in 1 country.

Miguel A Martín-AcebesDepartments of Virology and Microbiology Centro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Madrid 28049, Spain Department of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Madrid 28040, Spain.
Enrique Gabandé-RodríguezMolecular Neurobiology, Centro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Madrid 28049, Spain.
Ana M García-CabreroLaboratory of Neurology, Instituto de Investigación Sanitaria Fundación Jiménez Díaz, Madrid 28040, Spain.
Marina P SánchezLaboratory of Neurology, Instituto de Investigación Sanitaria Fundación Jiménez Díaz, Madrid 28040, Spain.
María Dolores LedesmaMolecular Neurobiology, Centro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Madrid 28049, Spain.
Francisco SobrinoDepartments of Virology and Microbiology Centro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Madrid 28049, Spain fsobrino@cbm.csic.es jcsaiz@inia.es.
Juan-Carlos SaizDepartment of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Madrid 28040, Spain fsobrino@cbm.csic.es jcsaiz@inia.es.
Centro de Biología Molecular Severo Ochoa · ESHospital Universitario Fundación Jiménez Díaz · ESInstituto Nacional de Investigación y Tecnología Agraria y Alimentaria · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Flaviviruses, such as the dengue virus and the West Nile virus (WNV), are arthropod-borne viruses that represent a global health problem. The flavivirus lifecycle is intimately connected to cellular lipids. Among the lipids co-opted by flaviviruses, we have focused on SM, an important component of cellular membranes particularly enriched in the nervous system. After infection with the neurotropic WNV, mice deficient in acid sphingomyelinase (ASM), which accumulate high levels of SM in their tissues, displayed exacerbated infection. In addition, WNV multiplication was enhanced in cells from human patients with Niemann-Pick type A, a disease caused by a deficiency of ASM activity resulting in SM accumulation. Furthermore, the addition of SM to cultured cells also increased WNV infection, whereas treatment with pharmacological inhibitors of SM synthesis reduced WNV infection. Confocal microscopy analyses confirmed the association of SM with viral replication sites within infected cells. Our results unveil that SM metabolism regulates flavivirus infection in vivo and propose SM as a suitable target for antiviral design against WNV.

Indexed as

Host-Pathogen InteractionsAnimalsBrainEndoplasmic ReticulumFemaleFibroblastsGene Knockout TechniquesHumansIntracellular MembranesMaleMiceMice, Inbred C57BLNiemann-Pick DiseasesSphingomyelin PhosphodiesteraseSphingomyelinsVirus ReplicationSphingomyelin PhosphodiesteraseSphingomyelinsbrain lipidsflaviviruslipidsNiemann-Pick diseasesphingolipidsstorage diseases

Identifiers

PMID26764042
PMCPMC4766991
OpenAlexW2236250998

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.