Enterovirus 71 virion-associated galectin-1 facilitates viral replication and stability

Pei Huan Lee, Chia Ming Liu, Tzong Shiann Ho, Yi Che Tsai, Chi Cheng Lin, Ya Fang Wang, Yuh Ling Chen, Chun Keung Yu, Shih Min Wang, Ching Chuan Liu, Ai Li Shiau, Huan Yao Lei, Chih Peng Chang

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Enterovirus 71 (EV71) infection causes a myriad of diseases from mild hand-foot-and-mouth disease or herpangina to fatal brain stem encephalitis complicated with pulmonary edema. Several severe EV71 endemics have occurred in Asia-Pacific region, including Taiwan, and have become a serious threat to children' s health. EV71 infection is initiated by the attachment of the virion to the target cell surface. Although this process relies primarily upon interaction between viruses and cell surface receptors, soluble factors may also influence the binding of EV71 to host cells.Galectin-1 has been reported to participate in several virus infections, but is not addressed in EV71. In this study, we found that the serum levels of galectin-1 in EV71-infected children were higher than those in non-infected people. In EV71 infected cells, galectin-1 was found to be associated with the EV71 VP1 and VP3 via carbohydrate residues and subsequently released and bound to another cell surface along with the virus. EV71 propagated from galectin-1 knockdown SK-N-SH cells exhibited lower infectivity in cultured cells and less pathogenicity in mice than the virus propagated from parental cells. In addition, this galectin-1-free EV71 virus was sensitive to high temperature and lost its viability after long-term storage, which could be restored following supplement of recombinant galectin-1. Taken together, our findings uncover a new role of galectin-1 in facilitating EV71 virus infection.

Original languageEnglish
Article numbere0116278
JournalPloS one
Volume10
Issue number2
DOIs
Publication statusPublished - 2015 Feb 23

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Galectin 1
Enterovirus
virus replication
virion
Virion
Viruses
viruses
Enterovirus Infections
Virus Diseases
cells
Herpangina
infection
Hand, Foot and Mouth Disease
Cell Surface Receptors
pathogenicity
hand, foot and mouth disease
Brain
Pulmonary Edema
Encephalitis
Taiwan

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

Cite this

@article{5e460059168742479f91637127e676c5,
title = "Enterovirus 71 virion-associated galectin-1 facilitates viral replication and stability",
abstract = "Enterovirus 71 (EV71) infection causes a myriad of diseases from mild hand-foot-and-mouth disease or herpangina to fatal brain stem encephalitis complicated with pulmonary edema. Several severe EV71 endemics have occurred in Asia-Pacific region, including Taiwan, and have become a serious threat to children' s health. EV71 infection is initiated by the attachment of the virion to the target cell surface. Although this process relies primarily upon interaction between viruses and cell surface receptors, soluble factors may also influence the binding of EV71 to host cells.Galectin-1 has been reported to participate in several virus infections, but is not addressed in EV71. In this study, we found that the serum levels of galectin-1 in EV71-infected children were higher than those in non-infected people. In EV71 infected cells, galectin-1 was found to be associated with the EV71 VP1 and VP3 via carbohydrate residues and subsequently released and bound to another cell surface along with the virus. EV71 propagated from galectin-1 knockdown SK-N-SH cells exhibited lower infectivity in cultured cells and less pathogenicity in mice than the virus propagated from parental cells. In addition, this galectin-1-free EV71 virus was sensitive to high temperature and lost its viability after long-term storage, which could be restored following supplement of recombinant galectin-1. Taken together, our findings uncover a new role of galectin-1 in facilitating EV71 virus infection.",
author = "Lee, {Pei Huan} and Liu, {Chia Ming} and Ho, {Tzong Shiann} and Tsai, {Yi Che} and Lin, {Chi Cheng} and Wang, {Ya Fang} and Chen, {Yuh Ling} and Yu, {Chun Keung} and Wang, {Shih Min} and Liu, {Ching Chuan} and Shiau, {Ai Li} and Lei, {Huan Yao} and Chang, {Chih Peng}",
year = "2015",
month = "2",
day = "23",
doi = "10.1371/journal.pone.0116278",
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Enterovirus 71 virion-associated galectin-1 facilitates viral replication and stability. / Lee, Pei Huan; Liu, Chia Ming; Ho, Tzong Shiann; Tsai, Yi Che; Lin, Chi Cheng; Wang, Ya Fang; Chen, Yuh Ling; Yu, Chun Keung; Wang, Shih Min; Liu, Ching Chuan; Shiau, Ai Li; Lei, Huan Yao; Chang, Chih Peng.

In: PloS one, Vol. 10, No. 2, e0116278, 23.02.2015.

Research output: Contribution to journalArticle

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AU - Lee, Pei Huan

AU - Liu, Chia Ming

AU - Ho, Tzong Shiann

AU - Tsai, Yi Che

AU - Lin, Chi Cheng

AU - Wang, Ya Fang

AU - Chen, Yuh Ling

AU - Yu, Chun Keung

AU - Wang, Shih Min

AU - Liu, Ching Chuan

AU - Shiau, Ai Li

AU - Lei, Huan Yao

AU - Chang, Chih Peng

PY - 2015/2/23

Y1 - 2015/2/23

N2 - Enterovirus 71 (EV71) infection causes a myriad of diseases from mild hand-foot-and-mouth disease or herpangina to fatal brain stem encephalitis complicated with pulmonary edema. Several severe EV71 endemics have occurred in Asia-Pacific region, including Taiwan, and have become a serious threat to children' s health. EV71 infection is initiated by the attachment of the virion to the target cell surface. Although this process relies primarily upon interaction between viruses and cell surface receptors, soluble factors may also influence the binding of EV71 to host cells.Galectin-1 has been reported to participate in several virus infections, but is not addressed in EV71. In this study, we found that the serum levels of galectin-1 in EV71-infected children were higher than those in non-infected people. In EV71 infected cells, galectin-1 was found to be associated with the EV71 VP1 and VP3 via carbohydrate residues and subsequently released and bound to another cell surface along with the virus. EV71 propagated from galectin-1 knockdown SK-N-SH cells exhibited lower infectivity in cultured cells and less pathogenicity in mice than the virus propagated from parental cells. In addition, this galectin-1-free EV71 virus was sensitive to high temperature and lost its viability after long-term storage, which could be restored following supplement of recombinant galectin-1. Taken together, our findings uncover a new role of galectin-1 in facilitating EV71 virus infection.

AB - Enterovirus 71 (EV71) infection causes a myriad of diseases from mild hand-foot-and-mouth disease or herpangina to fatal brain stem encephalitis complicated with pulmonary edema. Several severe EV71 endemics have occurred in Asia-Pacific region, including Taiwan, and have become a serious threat to children' s health. EV71 infection is initiated by the attachment of the virion to the target cell surface. Although this process relies primarily upon interaction between viruses and cell surface receptors, soluble factors may also influence the binding of EV71 to host cells.Galectin-1 has been reported to participate in several virus infections, but is not addressed in EV71. In this study, we found that the serum levels of galectin-1 in EV71-infected children were higher than those in non-infected people. In EV71 infected cells, galectin-1 was found to be associated with the EV71 VP1 and VP3 via carbohydrate residues and subsequently released and bound to another cell surface along with the virus. EV71 propagated from galectin-1 knockdown SK-N-SH cells exhibited lower infectivity in cultured cells and less pathogenicity in mice than the virus propagated from parental cells. In addition, this galectin-1-free EV71 virus was sensitive to high temperature and lost its viability after long-term storage, which could be restored following supplement of recombinant galectin-1. Taken together, our findings uncover a new role of galectin-1 in facilitating EV71 virus infection.

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