Evidence map›Paper›PMID 31053158›Full record

ArticleCell communication and signaling : CCS2019

Zika virus: mapping and reprogramming the entry.

Katarzyna Owczarek, Yuliya Chykunova, Christian Jassoy, Beata Maksym, Zenon Rajfur, Krzysztof Pyrc

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.2field-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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Article
  6. Virus infection and vesicle trafficking.Frontiers in immunology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. An overview of Zika virus genotypes and their infectivity.Revista da Sociedade Brasileira de Medicina Tropical · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. Review
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 2 institutions in 1 country.

Katarzyna OwczarekVirogenetics Laboratory of Virology, Malopolska Centre of Biotechnology, Jagiellonian University, Gronostajowa,7a 2.25, 30-387, Krakow, Poland.
Yuliya ChykunovaMicrobiology Department, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Gronostajowa 7, 30-387, Krakow, Poland.
Christian JassoyInstitute for Virology, University Clinics and Medical Faculty, University of Leipzig, Leipzig, Germany.
Beata MaksymDepartment of Pharmacology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia in Katowice, Zabrze, Poland.
Zenon RajfurInstitute of Physics, Faculty of Physics, Astronomy and Applied Computer Sciences, Jagiellonian University, Lojasiewicza 11, 30-348, Krakow, Poland.
Krzysztof PyrcVirogenetics Laboratory of Virology, Malopolska Centre of Biotechnology, Jagiellonian University, Gronostajowa,7a 2.25, 30-387, Krakow, Poland. k.a.pyrc@uj.edu.pl.ORCID 0000-0002-3867-7688
Jagiellonian University · PLMedical University of Silesia · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe flaviviridae family comprises single-stranded RNA viruses that enter cells via clathrin-mediated pH-dependent endocytosis. Although the initial events of the virus entry have been already identified, data regarding intracellular virus trafficking and delivery to the replication site are limited. The purpose of this study was to map the transport route of Zika virus and to identify the fusion site within the endosomal compartment.

methodsTracking of viral particles in the cell was carried out with confocal microscopy. Immunostaining of two structural proteins of Zika virus enabled precise mapping of the route of the ribonucleocapsid and the envelope and, consequently, mapping the fusion site in the endosomal compartment. The results were verified using RNAi silencing and chemical inhibitors.

resultsAfter endocytic internalization, Zika virus is trafficked through the endosomal compartment to fuse in late endosomes. Inhibition of endosome acidification using bafilomycin A1 hampers the infection, as the fusion is inhibited; instead, the virus is transported to late compartments where it undergoes proteolytic degradation. The degradation products are ejected from the cell via slow recycling vesicles. Surprisingly, NH

conclusionsZika virus fusion occurs in late endosomes and is pH-dependent. These results broaden our understanding of Zika virus intracellular trafficking and may in future allow for development of novel treatment strategies. Further, we identified a novel mode of action for agents commonly used in studies of virus entry. Schematic representation of differences in ZIKV trafficking in the presence of Baf A1 and NH

Indexed as

Virus InternalizationAnimalsChlorocebus aethiopsEndosomesEnzyme InhibitorsMacrolidesVero CellsZika Virusbafilomycin A1Enzyme InhibitorsMacrolidesAmmonium chlorideBafilomycin A1EndocytosisFurinRecyclingTraffickingZIKV

Identifiers

PMID31053158
PMCPMC6500006
OpenAlexW2946841087

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.