Please use this identifier to cite or link to this item: https://doi.org/10.1080/22221751.2019.1590130
Title: Cell surface alpha 2,3-linked sialic acid facilitates Zika virus internalization
Authors: Tan, Chee Wah 
Hor, Catherine Hong Huan 
Kwek, Swee Sen
Tee, Han Kang
Sam, I-Ching
Goh, Eyleen LK 
Ooi, Eng Eong 
Chan, Yoke Fun
Wang, Lin-Fa 
Keywords: Science & Technology
Life Sciences & Biomedicine
Immunology
Microbiology
Zika virus
flavivirus
sialic acid
neural progenitor cells
internalization
ENVELOPE PROTEIN
HEPARAN-SULFATE
C6/36 CELLS
INFECTION
DENGUE
BINDING
AXL
IDENTIFICATION
RECEPTORS
EFFICIENCY
Issue Date: 22-Mar-2019
Publisher: TAYLOR & FRANCIS LTD
Citation: Tan, Chee Wah, Hor, Catherine Hong Huan, Kwek, Swee Sen, Tee, Han Kang, Sam, I-Ching, Goh, Eyleen LK, Ooi, Eng Eong, Chan, Yoke Fun, Wang, Lin-Fa (2019-03-22). Cell surface alpha 2,3-linked sialic acid facilitates Zika virus internalization. EMERGING MICROBES & INFECTIONS 8 (1) : 426-437. ScholarBank@NUS Repository. https://doi.org/10.1080/22221751.2019.1590130
Abstract: © 2019, © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group, on behalf of Shanghai Shangyixun Cultural Communication Co., Ltd. The emergence of neurotropic Zika virus (ZIKV) raised a public health emergency of global concern. ZIKV can cross the placental barrier and infect foetal brains, resulting in microcephaly, but the pathogenesis of ZIKV is poorly understood. With recent findings reporting AXL as a type I interferon antagonist rather than an entry receptor, the exact entry mechanism remains unresolved. Here we report that cell surface sialic acid plays an important role in ZIKV infection. Removal of cell surface sialic acid by neuraminidase significantly abolished ZIKV infection in Vero cells and human induced-pluripotent stem cells-derived neural progenitor cells. Furthermore, knockout of the sialic acid biosynthesis gene encoding UDP-N-acetylglucosamine-2-epimerase/N-acetylmannosamine kinase resulted in significantly less ZIKV infection of both African and Asian lineages. Huh7 cells deficient in α2,3-linked sialic acid through knockout of ST3 β-galactoside-α2,3-sialyltransferase 4 had significantly reduced ZIKV infection. Removal of membrane-bound, un-internalized virus with pronase treatment revealed the role of sialic acid in ZIKV internalization but not attachment. Sialyllactose inhibition studies showed that there is no direct interaction between sialic acid and ZIKV, implying that sialic acid could be mediating ZIKV-receptor complex internalization. Identification of α2,3-linked sialic acid as an important host factor for ZIKV internalization provides new insight into ZIKV infection and pathogenesis.
Source Title: EMERGING MICROBES & INFECTIONS
URI: https://scholarbank.nus.edu.sg/handle/10635/155135
ISSN: 2222-1751
2222-1751
DOI: 10.1080/22221751.2019.1590130
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