Dual roles of exostosin glycosyltransferase 1 in Zika virus infection

Many factors involved in heparan sulfate (HS) biosynthesis and metabolism have been reported to play roles in viral infection. However, the detailed mechanisms are still not fully understood. In this study, we report that exostosin glycosyltransferase 1 (EXT1), the HS polymerase, is a critical regul...

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Main Authors: Jiaxin Ling, Asifa Khan, Matthias Denkewitz, Marco Maccarana, Åke Lundkvist, Jin-Ping Li, Jinlin Li
Format: Article
Language:English
Published: Taylor & Francis Group 2025-12-01
Series:Virulence
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Online Access:https://www.tandfonline.com/doi/10.1080/21505594.2025.2458681
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author Jiaxin Ling
Asifa Khan
Matthias Denkewitz
Marco Maccarana
Åke Lundkvist
Jin-Ping Li
Jinlin Li
author_facet Jiaxin Ling
Asifa Khan
Matthias Denkewitz
Marco Maccarana
Åke Lundkvist
Jin-Ping Li
Jinlin Li
author_sort Jiaxin Ling
collection DOAJ
description Many factors involved in heparan sulfate (HS) biosynthesis and metabolism have been reported to play roles in viral infection. However, the detailed mechanisms are still not fully understood. In this study, we report that exostosin glycosyltransferase 1 (EXT1), the HS polymerase, is a critical regulatory factor for Zika virus (ZIKV) infection. Knocking out EXT1 dramatically restricts ZIKV infection, which is not due to the inhibition of virus entry resulting from HS deficiency, but mediated by the downregulation of autophagy. Induction of autophagy promotes ZIKV infection, and attenuated autophagy is found in distinct EXT1 knockout (EXT1-KO) cell lines. Induction of autophagy by rapamycin can relieve the ZIKV production defect in EXT1-KO cells. While over-expressing EXT1 results in the reduction of ZIKV production by targeting the viral envelope (E) protein and non-structural protein NS3 in a proteasome-dependent degradation manner. The different roles of EXT1 in ZIKV infection are further confirmed by the data that knocking down EXT1 at the early stage of ZIKV infection represses viral infection, whereas the increase of ZIKV infection is observed when knocking down EXT1 at the late stage of viral infection. This study discovers previously unrecognized intricate roles of EXT1 in ZIKV infection.
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spelling doaj-art-e42ce05ed3d2422cb9388f8d37271ea62025-08-20T03:12:14ZengTaylor & Francis GroupVirulence2150-55942150-56082025-12-0116110.1080/21505594.2025.2458681Dual roles of exostosin glycosyltransferase 1 in Zika virus infectionJiaxin Ling0Asifa Khan1Matthias Denkewitz2Marco Maccarana3Åke Lundkvist4Jin-Ping Li5Jinlin Li6Department of Medical Biochemistry and Microbiology, The Biomedical Center, Uppsala University, Uppsala, SwedenDepartment of Medical Biochemistry and Microbiology, The Biomedical Center, Uppsala University, Uppsala, SwedenDepartment of Medical Biochemistry and Microbiology, The Biomedical Center, Uppsala University, Uppsala, SwedenDepartment of Medical Biochemistry and Microbiology, The Biomedical Center, Uppsala University, Uppsala, SwedenDepartment of Medical Biochemistry and Microbiology, The Biomedical Center, Uppsala University, Uppsala, SwedenDepartment of Medical Biochemistry and Microbiology, The Biomedical Center, Uppsala University, Uppsala, SwedenDepartment of Medical Biochemistry and Microbiology, The Biomedical Center, Uppsala University, Uppsala, SwedenMany factors involved in heparan sulfate (HS) biosynthesis and metabolism have been reported to play roles in viral infection. However, the detailed mechanisms are still not fully understood. In this study, we report that exostosin glycosyltransferase 1 (EXT1), the HS polymerase, is a critical regulatory factor for Zika virus (ZIKV) infection. Knocking out EXT1 dramatically restricts ZIKV infection, which is not due to the inhibition of virus entry resulting from HS deficiency, but mediated by the downregulation of autophagy. Induction of autophagy promotes ZIKV infection, and attenuated autophagy is found in distinct EXT1 knockout (EXT1-KO) cell lines. Induction of autophagy by rapamycin can relieve the ZIKV production defect in EXT1-KO cells. While over-expressing EXT1 results in the reduction of ZIKV production by targeting the viral envelope (E) protein and non-structural protein NS3 in a proteasome-dependent degradation manner. The different roles of EXT1 in ZIKV infection are further confirmed by the data that knocking down EXT1 at the early stage of ZIKV infection represses viral infection, whereas the increase of ZIKV infection is observed when knocking down EXT1 at the late stage of viral infection. This study discovers previously unrecognized intricate roles of EXT1 in ZIKV infection.https://www.tandfonline.com/doi/10.1080/21505594.2025.2458681ZIKVEXT1heparan sulfateautophagy
spellingShingle Jiaxin Ling
Asifa Khan
Matthias Denkewitz
Marco Maccarana
Åke Lundkvist
Jin-Ping Li
Jinlin Li
Dual roles of exostosin glycosyltransferase 1 in Zika virus infection
Virulence
ZIKV
EXT1
heparan sulfate
autophagy
title Dual roles of exostosin glycosyltransferase 1 in Zika virus infection
title_full Dual roles of exostosin glycosyltransferase 1 in Zika virus infection
title_fullStr Dual roles of exostosin glycosyltransferase 1 in Zika virus infection
title_full_unstemmed Dual roles of exostosin glycosyltransferase 1 in Zika virus infection
title_short Dual roles of exostosin glycosyltransferase 1 in Zika virus infection
title_sort dual roles of exostosin glycosyltransferase 1 in zika virus infection
topic ZIKV
EXT1
heparan sulfate
autophagy
url https://www.tandfonline.com/doi/10.1080/21505594.2025.2458681
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