ArticlePloS one2014
Zebrafish 3-O-sulfotransferase-4 generated heparan sulfate mediates HSV-1 entry and spread.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Zebrafish as a model organism for virus disease research: Current status and future directions.Heliyon · 2024Article
- Plant Cell-Engineered Gold Nanoparticles Conjugated to Quercetin Inhibit SARS-CoV-2 and HSV-1 Entry.International journal of molecular sciences · 2023Article
- Archaic connectivity between the sulfated heparan sulfate and the herpesviruses - An evolutionary potential for cross-species interactions.Computational and structural biotechnology journal · 2023Review
- Synthesis of 3-ACS chemical biology · 2021Article
- Modeling Virus-Induced Inflammation in Zebrafish: A Balance Between Infection Control and Excessive Inflammation.Frontiers in immunology · 2021Review
- 3-O-sulfated heparan sulfate interactors target synaptic adhesion molecules from neonatal mouse brain and inhibit neural activity and synaptogenesis in vitro.Scientific reports · 2020Article
- Comparative Genomic Analysis of Three Salmonid Species Identifies Functional Candidate Genes Involved in Resistance to the Intracellular BacteriumFrontiers in genetics · 2019Article
- HS3ST2 expression is critical for the abnormal phosphorylation of tau in Alzheimer's disease-related tau pathology.Brain : a journal of neurology · 2015Article
- Diversity of heparan sulfate and HSV entry: basic understanding and treatment strategies.Molecules (Basel, Switzerland) · 2015Review
- Comprehensive analysis of herpes simplex virus 1 (HSV-1) entry mediated by zebrafish 3-O-Sulfotransferase isoforms: implications for the development of a zebrafish model of HSV-1 infection.Journal of virology · 2014Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Rare modification of heparan sulfate (HS) by glucosaminyl 3-O sulfotransferase (3-OST) isoforms generates an entry receptor for herpes simplex virus type-1 (HSV-1). In the zebrafish (ZF) model multiple 3-OST isoforms are differentially expressed. One such isoform is 3-OST-4 which is widely expressed in the central nervous system of ZF. In this report we characterize the role of ZF encoded 3-OST-4 isoform for HSV-1 entry. Expression of ZF 3-OST-4 into resistant Chinese hamster ovary (CHO-K1) cells promoted susceptibility to HSV-1 infection. This entry was 3-O sulfated HS (3-OS HS) dependent as pre-treatment of ZF 3-OST-4 cells with enzyme HS lyases (heparinase II/III) significantly reduced HSV-1 entry. Interestingly, co-expression of ZF 3-OST-4 along with ZF 3-OST-2 which is also expressed in brain rendered cells more susceptible to HSV-1 than 3-OST-4 alone. The role of ZF-3-OST-4 in the spread of HSV-1 was also evaluated as CHO-K1 cells that expressed HSV-1 glycoproteins fused with ZF 3-OST-4 expressing effector CHO-K1 cells. Finally, adding further evidence ZF 3-OST-4 mediated HSV-1 entry was inhibited by anti-3O HS G2 peptide. Taken together our results demonstrate a role for ZF 3-OST-4 in HSV-1 pathogenesis and support the use of ZF as a model to study it.
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