Evidence map›Paper›PMID 30044839›Full record

ArticlePloS one2018

Dengue immune sera enhance Zika virus infection in human peripheral blood monocytes through Fc gamma receptors.

Min Li, Lingzhai Zhao, Chao Zhang, Xin Wang, Wenxin Hong, Jin Sun, Ran Liu, Lei Yu, Jianhua Wang, Fuchun Zhang and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. 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
4.4field-weighted citation impact, top 6% 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, 27 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

11 authors at 3 institutions in 1 country.

Min LiCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences (CAS), Shanghai, China.
Lingzhai ZhaoGuangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
Chao ZhangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences (CAS), Shanghai, China.
Xin WangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences (CAS), Shanghai, China.
Wenxin HongGuangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
Jin SunCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences (CAS), Shanghai, China.
Ran LiuCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences (CAS), Shanghai, China.
Lei YuGuangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
Jianhua WangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences (CAS), Shanghai, China.
Fuchun ZhangGuangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
Xia JinCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences (CAS), Shanghai, China.
Chinese Academy of Sciences · CNGuangzhou Eighth People's Hospital · CNInstitut Pasteur of Shanghai · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibody dependent enhancement (ADE) has most often been associated with dengue virus (DENV). Studies using leukemia cell lines suggest that DENV specific antibodies can enhance Zika virus (ZIKV) infectivity, and vice versa. To examine the mechanisms of ADE of ZIKV infection in primary human cells, we assessed 40 serum samples obtained from convalescent DENV-1 or DENV-3 infected subjects. All sera tested exhibited high binding potency, while modest or none neutralization activities against ZIKV. Primary CD14+ monocytes, rather than B and T cells in peripheral blood mononuclear cells (PBMCs), were found to be the mediators of the enhancement of ZIKV infectivity by DENV immune sera. Monocyte-derived immature dendritic cells (DCs), but not mature DCs were highly permissive to ZIKV infection, whereas neither immature nor mature DCs could mediate enhanced ZIKV infection in the presence of DENV immune sera. In addition, antibody blocking of either FcγRI (CD64), or FcγRII (CD32), or FcγRIII (CD16) resulted in diminished ADE of ZIKV infection. Our findings provide an improved understanding of the pathogenesis of ZIKV infection, and inform rational vaccine design.

Indexed as

AdolescentAdultAgedAntibodies, ViralAntibody-Dependent EnhancementCross ReactionsDendritic CellsDengueDengue VirusFemaleHumansImmune SeraMaleMiddle AgedMonocytesNeutralization TestsAntibodies, ViralImmune SeraReceptors, IgG

Identifiers

PMID30044839
PMCPMC6059439
OpenAlexW2883755085

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.