Timing of galectin-1 exposure differentially modulates Nipah virus entry and syncytium formation in endothelial cells

Omai B. Garner, Tatyana Yun, Olivier Pernet, Hector C. Aguilar, Arnold Park, Thomas A. Bowden, Alexander Freiberg, Benhur Lee, Linda G. Baum

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Nipah virus (NiV) is a deadly emerging enveloped paramyxovirus that primarily targets human endothelial cells. Endothelial cells express the innate immune effector galectin-1 that we have previously shown can bind to specific N-glycans on the NiV envelope fusion glycoprotein (F). NiV-F mediates fusion of infected endothelial cells into syncytia, resulting in endothelial disruption and hemorrhage. Galectin-1 is an endogenous carbohydrate-binding protein that binds to specific glycans on NiV-F to reduce endothelial cell fusion, an effect that may reduce pathophysiologic sequelae of NiV infection. However, galectins play multiple roles in regulating host-pathogen interactions; for example, galectins can promote attachment of HIV to T cells and macrophages and attachment of HSV-1 to keratinocytes but can also inhibit influenza entry into airway epithelial cells. Using live Nipah virus, in the present study, we demonstrate that galectin-1 can enhance NiV attachment to and infection of primary human endothelial cells by bridging glycans on the viral envelope to host cell glycoproteins. In order to exhibit an enhancing effect, galectin-1 must be present during the initial phase of virus attachment; in contrast, addition of galectin-1 postinfection results in reduced production of progeny virus and syncytium formation. Thus, galectin-1 can have dual and opposing effects on NiV infection of human endothelial cells. While various roles for galectin family members in microbial-host interactions have been described, we report opposing effects of the same galectin family member on a specific virus, with the timing of exposure during the viral life cycle determining the outcome.

Original languageEnglish (US)
Pages (from-to)2520-2529
Number of pages10
JournalJournal of Virology
Volume89
Issue number5
DOIs
StatePublished - 2015

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Nipah Virus
Nipah virus
Galectin 1
Virus Internalization
giant cells
Giant Cells
endothelial cells
Endothelial Cells
Galectins
Virus Diseases
Polysaccharides
Virus Attachment
polysaccharides
viruses
glycoproteins
Glycoproteins
Microbial Interactions
infection
Viruses
Respirovirus

ASJC Scopus subject areas

  • Immunology
  • Virology

Cite this

Garner, O. B., Yun, T., Pernet, O., Aguilar, H. C., Park, A., Bowden, T. A., ... Baum, L. G. (2015). Timing of galectin-1 exposure differentially modulates Nipah virus entry and syncytium formation in endothelial cells. Journal of Virology, 89(5), 2520-2529. https://doi.org/10.1128/JVI.02435-14

Timing of galectin-1 exposure differentially modulates Nipah virus entry and syncytium formation in endothelial cells. / Garner, Omai B.; Yun, Tatyana; Pernet, Olivier; Aguilar, Hector C.; Park, Arnold; Bowden, Thomas A.; Freiberg, Alexander; Lee, Benhur; Baum, Linda G.

In: Journal of Virology, Vol. 89, No. 5, 2015, p. 2520-2529.

Research output: Contribution to journalArticle

Garner, OB, Yun, T, Pernet, O, Aguilar, HC, Park, A, Bowden, TA, Freiberg, A, Lee, B & Baum, LG 2015, 'Timing of galectin-1 exposure differentially modulates Nipah virus entry and syncytium formation in endothelial cells', Journal of Virology, vol. 89, no. 5, pp. 2520-2529. https://doi.org/10.1128/JVI.02435-14
Garner, Omai B. ; Yun, Tatyana ; Pernet, Olivier ; Aguilar, Hector C. ; Park, Arnold ; Bowden, Thomas A. ; Freiberg, Alexander ; Lee, Benhur ; Baum, Linda G. / Timing of galectin-1 exposure differentially modulates Nipah virus entry and syncytium formation in endothelial cells. In: Journal of Virology. 2015 ; Vol. 89, No. 5. pp. 2520-2529.
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