Evidence map›Paper›PMID 30898036›Full record

ArticleEmerging microbes & infections2019

Cell surface α2,3-linked sialic acid facilitates Zika virus internalization.

Chee Wah Tan, Catherine Hong Huan Hor, Swee Sen Kwek, Han Kang Tee, I-Ching Sam, Eyleen L K Goh, Eng Eong Ooi, Yoke Fun Chan, Lin-Fa Wang

Open access · goldAbstract read
In one paragraph

Article in Emerging microbes & infections, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.0field-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

29 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Advances in immunological research on male infertility.Frontiers in reproductive health · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Testicular immunity.Molecular aspects of medicine · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Advancement in the Development of Therapeutics Against Zika Virus Infection.Frontiers in cellular and infection microbiology · 2022
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article
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

9 authors at 3 institutions in 2 countries.

Chee Wah Tana Programme in Emerging Infectious Diseases , Duke-NUS Medical School , Singapore , Singapore.
Catherine Hong Huan Horb Neuroscience Academic Clinical Programme , Duke-NUS Medical School , Singapore , Singapore.ORCID http://orcid.org/0000-0002-7467-2243
Swee Sen Kweka Programme in Emerging Infectious Diseases , Duke-NUS Medical School , Singapore , Singapore.
Han Kang Teec Department of Medical Microbiology, Faculty of Medicine , University of Malaya , Kuala Lumpur , Malaysia.
I-Ching Samc Department of Medical Microbiology, Faculty of Medicine , University of Malaya , Kuala Lumpur , Malaysia.
Eyleen L K Gohb Neuroscience Academic Clinical Programme , Duke-NUS Medical School , Singapore , Singapore.
Eng Eong Ooia Programme in Emerging Infectious Diseases , Duke-NUS Medical School , Singapore , Singapore.
Yoke Fun Chanc Department of Medical Microbiology, Faculty of Medicine , University of Malaya , Kuala Lumpur , Malaysia.
Lin-Fa Wanga Programme in Emerging Infectious Diseases , Duke-NUS Medical School , Singapore , Singapore.ORCID http://orcid.org/0000-0003-2752-0535
Duke-NUS Medical School · SGUniversity Malaya Medical Centre · MYSingHealth Duke-NUS Academic Medical Centre · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The emergence of neurotropic Zika virus (ZIKV) raised a public health emergency of global concern. ZIKV can cross the placental barrier and infect foetal brains, resulting in microcephaly, but the pathogenesis of ZIKV is poorly understood. With recent findings reporting AXL as a type I interferon antagonist rather than an entry receptor, the exact entry mechanism remains unresolved. Here we report that cell surface sialic acid plays an important role in ZIKV infection. Removal of cell surface sialic acid by neuraminidase significantly abolished ZIKV infection in Vero cells and human induced-pluripotent stem cells-derived neural progenitor cells. Furthermore, knockout of the sialic acid biosynthesis gene encoding UDP-N-acetylglucosamine-2-epimerase/N-acetylmannosamine kinase resulted in significantly less ZIKV infection of both African and Asian lineages. Huh7 cells deficient in α2,3-linked sialic acid through knockout of ST3 β-galactoside-α2,3-sialyltransferase 4 had significantly reduced ZIKV infection. Removal of membrane-bound, un-internalized virus with pronase treatment revealed the role of sialic acid in ZIKV internalization but not attachment. Sialyllactose inhibition studies showed that there is no direct interaction between sialic acid and ZIKV, implying that sialic acid could be mediating ZIKV-receptor complex internalization. Identification of α2,3-linked sialic acid as an important host factor for ZIKV internalization provides new insight into ZIKV infection and pathogenesis.

Indexed as

Virus InternalizationAnimalsCell LineHumansN-Acetylneuraminic AcidReceptors, VirusZika VirusN-Acetylneuraminic AcidReceptors, Virusflavivirusinternalizationneural progenitor cellssialic acidZika virus

Identifiers

PMID30898036
PMCPMC6455136
OpenAlexW2922731288

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.