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
Department of Microbiology & Immunology, College of Medicine, National Cheng Kung University, Tainan, 701, Taiwan.
Department of Emergency Medicine, National Cheng Kung University Hospital, Tainan, 701, Taiwan; Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan, 701, Taiwan.
PLoS One. 2015 Feb 23;10(2):e0116278. doi: 10.1371/journal.pone.0116278. eCollection 2015.
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.
肠道病毒71型（EV71）感染可引发多种疾病，从轻度手足口病或疱疹性咽峡炎到伴有肺水肿的致命脑干脑炎。包括台湾地区在内的亚太地区已发生多起严重的EV71疫情，对儿童健康构成了严重威胁。EV71感染始于病毒粒子附着于靶细胞表面。虽然这一过程主要依赖病毒与细胞表面受体之间的相互作用，但可溶性因子也可能影响EV71与宿主细胞的结合。据报道，半乳糖凝集素-1参与了多种病毒感染，但在EV71感染方面尚未有相关研究。在本研究中，我们发现EV71感染儿童的血清半乳糖凝集素-1水平高于未感染人群。在EV71感染的细胞中，发现半乳糖凝集素-1通过碳水化合物残基与EV71的VP1和VP3相关联，随后与病毒一起释放并结合到另一个细胞表面。与从亲本细胞繁殖的病毒相比，从半乳糖凝集素-1基因敲低的SK-N-SH细胞繁殖的EV71在培养细胞中的感染性较低，在小鼠中的致病性也较低。此外，这种不含半乳糖凝集素-1的EV71病毒对高温敏感，长期储存后失去活力，补充重组半乳糖凝集素-1后可恢复活力。综上所述，我们的研究结果揭示了半乳糖凝集素-1在促进EV71病毒感染中的新作用。
