Sialylated glycans as receptor and inhibitor of enterovirus 71 infection to DLD-1 intestinal cells
Abstract Background Many viruses recognize specific sugar residues, particularly sulfated or sialylated glycans, as the infection receptors. A change of sialic acid (2-6)-linked galactose (SA-α2,6Gal) to SA-α2,3Gal determines the receptor for avian flu infection. The receptor for enterovirus 71 (EV7...
Main Authors: | , , |
---|---|
Format: | Other/Unknown Material |
Language: | English |
Published: |
BioMed Central Ltd.
2009
|
Subjects: | |
Online Access: | http://www.virologyj.com/content/6/1/141 |
id |
ftbiomed:oai:biomedcentral.com:1743-422X-6-141 |
---|---|
record_format |
openpolar |
spelling |
ftbiomed:oai:biomedcentral.com:1743-422X-6-141 2023-05-15T15:34:31+02:00 Sialylated glycans as receptor and inhibitor of enterovirus 71 infection to DLD-1 intestinal cells Yang, Betsy Chuang, Hau Yang, Kuender D 2009-09-15 http://www.virologyj.com/content/6/1/141 en eng BioMed Central Ltd. http://www.virologyj.com/content/6/1/141 Copyright 2009 Yang et al; licensee BioMed Central Ltd. Research 2009 ftbiomed 2009-09-26T02:57:02Z Abstract Background Many viruses recognize specific sugar residues, particularly sulfated or sialylated glycans, as the infection receptors. A change of sialic acid (2-6)-linked galactose (SA-α2,6Gal) to SA-α2,3Gal determines the receptor for avian flu infection. The receptor for enterovirus 71 (EV71) infection that frequently causes fatal encephalitis in Asian children remains unclear. Currently, there is no effective vaccine or anti-virus agent for EV71 infection. Using DLD-1 intestinal cells, this study investigated whether SA-linked glycan on DLD-1 intestinal cells was a receptor for EV71, and whether natural SA-linked sugars from human milk could block EV71 infection. Results EV71 specifically infected DLD-1 intestinal cells but not K562 myeloid cells. Depletion of O-linked glycans or glycolipids, but not N-linked glycans, significantly decreased EV71 infection of DLD-1 cells. Pretreatment of DLD-1 cells with sialidase (10 mU, 2 hours) significantly reduced 20-fold EV71 replication (p < 0.01). Taken together, these results suggest that SA-linked O-glycans and glycolipids, but not N-glycans, on DLD-1 cells were responsible for EV71 infection. Purified SA-α2,3Gal and SA-α2,6Gal from human milk significantly inhibited EV71 infection of DLD-1 cells, indicating terminal SA-linked glycans could be receptors and inhibitors of EV71 infection. Conclusion This is the first in the literature to demonstrate that EV71 uses SA-linked glycans as receptors for infection, and natural SA-linked glycans from human milk can protect intestinal cells from EV71 infection. Further studies will test how a SA-containing glycan can prevent EV71 in the future. Other/Unknown Material Avian flu BioMed Central |
institution |
Open Polar |
collection |
BioMed Central |
op_collection_id |
ftbiomed |
language |
English |
description |
Abstract Background Many viruses recognize specific sugar residues, particularly sulfated or sialylated glycans, as the infection receptors. A change of sialic acid (2-6)-linked galactose (SA-α2,6Gal) to SA-α2,3Gal determines the receptor for avian flu infection. The receptor for enterovirus 71 (EV71) infection that frequently causes fatal encephalitis in Asian children remains unclear. Currently, there is no effective vaccine or anti-virus agent for EV71 infection. Using DLD-1 intestinal cells, this study investigated whether SA-linked glycan on DLD-1 intestinal cells was a receptor for EV71, and whether natural SA-linked sugars from human milk could block EV71 infection. Results EV71 specifically infected DLD-1 intestinal cells but not K562 myeloid cells. Depletion of O-linked glycans or glycolipids, but not N-linked glycans, significantly decreased EV71 infection of DLD-1 cells. Pretreatment of DLD-1 cells with sialidase (10 mU, 2 hours) significantly reduced 20-fold EV71 replication (p < 0.01). Taken together, these results suggest that SA-linked O-glycans and glycolipids, but not N-glycans, on DLD-1 cells were responsible for EV71 infection. Purified SA-α2,3Gal and SA-α2,6Gal from human milk significantly inhibited EV71 infection of DLD-1 cells, indicating terminal SA-linked glycans could be receptors and inhibitors of EV71 infection. Conclusion This is the first in the literature to demonstrate that EV71 uses SA-linked glycans as receptors for infection, and natural SA-linked glycans from human milk can protect intestinal cells from EV71 infection. Further studies will test how a SA-containing glycan can prevent EV71 in the future. |
format |
Other/Unknown Material |
author |
Yang, Betsy Chuang, Hau Yang, Kuender D |
spellingShingle |
Yang, Betsy Chuang, Hau Yang, Kuender D Sialylated glycans as receptor and inhibitor of enterovirus 71 infection to DLD-1 intestinal cells |
author_facet |
Yang, Betsy Chuang, Hau Yang, Kuender D |
author_sort |
Yang, Betsy |
title |
Sialylated glycans as receptor and inhibitor of enterovirus 71 infection to DLD-1 intestinal cells |
title_short |
Sialylated glycans as receptor and inhibitor of enterovirus 71 infection to DLD-1 intestinal cells |
title_full |
Sialylated glycans as receptor and inhibitor of enterovirus 71 infection to DLD-1 intestinal cells |
title_fullStr |
Sialylated glycans as receptor and inhibitor of enterovirus 71 infection to DLD-1 intestinal cells |
title_full_unstemmed |
Sialylated glycans as receptor and inhibitor of enterovirus 71 infection to DLD-1 intestinal cells |
title_sort |
sialylated glycans as receptor and inhibitor of enterovirus 71 infection to dld-1 intestinal cells |
publisher |
BioMed Central Ltd. |
publishDate |
2009 |
url |
http://www.virologyj.com/content/6/1/141 |
genre |
Avian flu |
genre_facet |
Avian flu |
op_relation |
http://www.virologyj.com/content/6/1/141 |
op_rights |
Copyright 2009 Yang et al; licensee BioMed Central Ltd. |
_version_ |
1766364881602215936 |