Evidence map›Paper›PMID 33827950›Full record

ArticleJournal of virology2021

ApoA1 Neutralizes Proinflammatory Effects of Dengue Virus NS1 Protein and Modulates Viral Immune Evasion.

Diego R Coelho, Pedro H Carneiro, Lucas Mendes-Monteiro, Jonas N Conde, Iamara Andrade, Thu Cao, Diego Allonso, Michael White-Dibiasio, Richard J Kuhn, Ronaldo Mohana-Borges

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.5field-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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Dengue NS1 as a Driver of Immune-Mediated Pathogenesis.Tropical medicine and infectious disease · 2026
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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 5 institutions in 2 countries.

Diego R CoelhoLaboratório de Biotecnologia e Bioengenharia Estrutural, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Pedro H CarneiroLaboratório de Biotecnologia e Bioengenharia Estrutural, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Lucas Mendes-MonteiroLaboratório de Biotecnologia e Bioengenharia Estrutural, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Jonas N CondeDepartment of Microbiology and Immunology, Stony Brook University, Stony Brook, New York, USA.
Iamara AndradeFaculdade de Educação Tecnológica do Estado do Rio de Janeiro, Paracambi, Rio de Janeiro, Brazil.
Thu CaoDepartment of Biological Sciences, Purdue University, West Lafayette, Indiana, USA.
Diego AllonsoDepartamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Michael White-DibiasioAffinia Therapeutics Inc., Waltham, Massachusetts, USA.
Richard J KuhnDepartment of Biological Sciences, Purdue University, West Lafayette, Indiana, USA.
Ronaldo Mohana-BorgesLaboratório de Biotecnologia e Bioengenharia Estrutural, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Universidade Federal do Rio de Janeiro · BRPurdue University West Lafayette · USInstituto Superior de Educação do Rio de Janeiro · BRNorthwestern University · USStony Brook University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dengue is a mosquito-borne infectious disease that is highly endemic in tropical and subtropical countries. Symptomatic patients can rapidly progress to severe conditions of hemorrhage, plasma extravasation, and hypovolemic shock, which leads to death. The blood tests of patients with severe dengue typically reveal low levels of high-density lipoprotein (HDL), which is responsible for reverse cholesterol transport (RCT) and regulation of the lipid composition in peripheral tissues. It is well known that dengue virus (DENV) depends on membrane cholesterol rafts to infect and to replicate in mammalian cells. Here, we describe the interaction of DENV nonstructural protein 1 (NS1) with apolipoprotein A1 (ApoA1), which is the major protein component of HDL. NS1 is secreted by infected cells and can be found circulating in the serum of patients with the onset of symptoms. NS1 concentrations in plasma are related to dengue severity, which is attributed to immune evasion and an acute inflammatory response. Our data show that the DENV NS1 protein induces an increase of lipid rafts in noninfected cell membranes and enhances further DENV infection. We also show that ApoA1-mediated lipid raft depletion inhibits DENV attachment to the cell surface. In addition, ApoA1 is able to neutralize NS1-induced cell activation and to prevent NS1-mediated enhancement of DENV infection. Furthermore, we demonstrate that the ApoA1 mimetic peptide 4F is also capable of mediating lipid raft depletion to control DENV infection. Taken together, our results suggest the potential of RCT-based therapies for dengue treatment. These results should motivate studies to assess the importance of RCT in DENV infection

Indexed as

AnimalsAntiviral AgentsApolipoprotein A-ICell LineCholesterolDengueDengue VirusHumansImmune EvasionInflammationMembrane MicrodomainsMicePeptidesRAW 264.7 CellsViral Nonstructural ProteinsVirus AttachmentAntiviral AgentsApoa1 protein, mouseApolipoprotein A-Iapolipoprotein A-I mimetic peptide 4FCholesterolNS1 protein, dengue-1 virusPeptidesViral Nonstructural Proteinsapolipoprotein A1dengue virusimmune evasionnonstructural 1 proteinprotein-protein interactions

Identifiers

PMID33827950
PMCPMC8437349
OpenAlexW3141234882

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.