Evidence map›Paper›PMID 35163212›Full record

ReviewInternational journal of molecular sciences2022

Apoptosis during ZIKA Virus Infection: Too Soon or Too Late?

Jonathan Turpin, Daed El Safadi, Grégorie Lebeau, Morgane Krejbich, Camille Chatelain, Philippe Desprès, Wildriss Viranaïcken, Pascale Krejbich-Trotot

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  9. Article
  10. An Overview of Zika Virus and Zika Virus Induced Neuropathies.International journal of molecular sciences · 2024
    Review
  11. Article
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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 2 countries.

Jonathan TurpinProcessus Infectieux en Milieu Insulaire Tropical (PIMIT), Université de La Réunion, INSERM UMR 1187, CNRS 9192, IRD 249, Plateforme CYROI, 97490 Sainte-Clotilde, France.ORCID 0000-0003-2667-345X
Daed El SafadiProcessus Infectieux en Milieu Insulaire Tropical (PIMIT), Université de La Réunion, INSERM UMR 1187, CNRS 9192, IRD 249, Plateforme CYROI, 97490 Sainte-Clotilde, France.
Grégorie LebeauProcessus Infectieux en Milieu Insulaire Tropical (PIMIT), Université de La Réunion, INSERM UMR 1187, CNRS 9192, IRD 249, Plateforme CYROI, 97490 Sainte-Clotilde, France.ORCID 0000-0002-9664-3486
Morgane KrejbichCRCI2NA, Centre de Recherche en Cancérologie et Immunologie, Université de Nantes, Université d'Angers, INSERM UMR 1307, 44000 Nantes, France.
Camille ChatelainCRCI2NA, Centre de Recherche en Cancérologie et Immunologie, Université de Nantes, Université d'Angers, INSERM UMR 1307, 44000 Nantes, France.
Philippe DesprèsProcessus Infectieux en Milieu Insulaire Tropical (PIMIT), Université de La Réunion, INSERM UMR 1187, CNRS 9192, IRD 249, Plateforme CYROI, 97490 Sainte-Clotilde, France.ORCID 0000-0001-8926-4050
Wildriss ViranaïckenProcessus Infectieux en Milieu Insulaire Tropical (PIMIT), Université de La Réunion, INSERM UMR 1187, CNRS 9192, IRD 249, Plateforme CYROI, 97490 Sainte-Clotilde, France.ORCID 0000-0002-0915-8635
Pascale Krejbich-TrototProcessus Infectieux en Milieu Insulaire Tropical (PIMIT), Université de La Réunion, INSERM UMR 1187, CNRS 9192, IRD 249, Plateforme CYROI, 97490 Sainte-Clotilde, France.ORCID 0000-0001-7329-1716
Centre National de la Recherche Scientifique · FRInserm · FR

Funding

ZIKAlert project (European Union-Région Réunion program under grant agreement n° SYNERGY: RE0001902) n° SYNERGY: RE0001902
6 · The paper itself

Abstract

Cell death by apoptosis is a major cellular response in the control of tissue homeostasis and as a defense mechanism in the case of cellular aggression such as an infection. Cell self-destruction is part of antiviral responses, aimed at limiting the spread of a virus. Although it may contribute to the deleterious effects in infectious pathology, apoptosis remains a key mechanism for viral clearance and the resolution of infection. The control mechanisms of cell death processes by viruses have been extensively studied. Apoptosis can be triggered by different viral determinants through different pathways as a result of virally induced cell stresses and innate immune responses. Zika virus (ZIKV) induces Zika disease in humans, which has caused severe neurological forms, birth defects, and microcephaly in newborns during the last epidemics. ZIKV also surprised by revealing an ability to persist in the genital tract and in semen, thus being sexually transmitted. Mechanisms of diverting antiviral responses such as the interferon response, the role of cytopathic effects and apoptosis in the etiology of the disease have been widely studied and debated. In this review, we examined the interplay between ZIKV infection of different cell types and apoptosis and how the virus deals with this cellular response. We illustrate a duality in the effects of ZIKV-controlled apoptosis, depending on whether it occurs too early or too late, respectively, in neuropathogenesis, or in long-term viral persistence. We further discuss a prospective role for apoptosis in ZIKV-related therapies, and the use of ZIKV as an oncolytic agent.

Indexed as

AnimalsAntiviral AgentsApoptosisCell DeathHost-Pathogen InteractionsHumansImmunity, InnateInterferonsMicrocephalyVirus Physiological PhenomenaVirus ReplicationZika VirusZika Virus InfectionAntiviral AgentsInterferonsapoptosiscell deathZika virusZIKV

Identifiers

PMID35163212
PMCPMC8835863
OpenAlexW4210247638

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.