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Axl Mediates ZIKA Virus Entry in Human Glial Cells and Modulates Innate Immune Responses

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Title: Axl Mediates ZIKA Virus Entry in Human Glial Cells and Modulates Innate Immune Responses
Authors: Laurent Meertens, Athena Labeau, Ophelie Dejarnac, Sara Cipriani, Laura Sinigaglia, Lucie Bonnet-Madin, Tifenn Le Charpentier, Mohamed Lamine Hafirassou, Alessia Zamborlini, Van-Mai Cao-Lormeau, Muriel Coulpier, Dorothée Missé, Nolwenn Jouvenet, Ray Tabibiazar, Pierre Gressens, Olivier Schwartz, Ali Amara
Source: Cell Reports, Vol 18, Iss 2, Pp 324-333 (2017)
Publisher Information: Elsevier, 2017.
Publication Year: 2017
Collection: LCC:Biology (General)
Subject Terms: Biology (General), QH301-705.5
More Details: Summary: ZIKA virus (ZIKV) is an emerging pathogen responsible for neurological disorders and congenital microcephaly. However, the molecular basis for ZIKV neurotropism remains poorly understood. Here, we show that Axl is expressed in human microglia and astrocytes in the developing brain and that it mediates ZIKV infection of glial cells. Axl-mediated ZIKV entry requires the Axl ligand Gas6, which bridges ZIKV particles to glial cells. Following binding, ZIKV is internalized through clathrin-mediated endocytosis and traffics to Rab5+ endosomes to establish productive infection. During entry, the ZIKV/Gas6 complex activates Axl kinase activity, which downmodulates interferon signaling and facilitates infection. ZIKV infection of human glial cells is inhibited by MYD1, an engineered Axl decoy receptor, and by the Axl kinase inhibitor R428. Our results highlight the dual role of Axl during ZIKV infection of glial cells: promoting viral entry and modulating innate immune responses. Therefore, inhibiting Axl function may represent a potential target for future antiviral therapies. : ZIKA virus (ZIKV) is responsible for congenital microcephaly. Meertens et al. show that the Axl receptor is expressed in microglia and astrocytes in the human developing brain. They also highlight the dual role of Axl during infection, which promotes viral entry and dampens innate immune responses in glial cells.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2211-1247
Relation: http://www.sciencedirect.com/science/article/pii/S2211124716317521; https://doaj.org/toc/2211-1247
DOI: 10.1016/j.celrep.2016.12.045
Access URL: https://doaj.org/article/4ff25352305542fb85ad301d2551bcc3
Accession Number: edsdoj.4ff25352305542fb85ad301d2551bcc3
Database: Directory of Open Access Journals
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  Data: Axl Mediates ZIKA Virus Entry in Human Glial Cells and Modulates Innate Immune Responses
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  Data: Cell Reports, Vol 18, Iss 2, Pp 324-333 (2017)
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  Data: Summary: ZIKA virus (ZIKV) is an emerging pathogen responsible for neurological disorders and congenital microcephaly. However, the molecular basis for ZIKV neurotropism remains poorly understood. Here, we show that Axl is expressed in human microglia and astrocytes in the developing brain and that it mediates ZIKV infection of glial cells. Axl-mediated ZIKV entry requires the Axl ligand Gas6, which bridges ZIKV particles to glial cells. Following binding, ZIKV is internalized through clathrin-mediated endocytosis and traffics to Rab5+ endosomes to establish productive infection. During entry, the ZIKV/Gas6 complex activates Axl kinase activity, which downmodulates interferon signaling and facilitates infection. ZIKV infection of human glial cells is inhibited by MYD1, an engineered Axl decoy receptor, and by the Axl kinase inhibitor R428. Our results highlight the dual role of Axl during ZIKV infection of glial cells: promoting viral entry and modulating innate immune responses. Therefore, inhibiting Axl function may represent a potential target for future antiviral therapies. : ZIKA virus (ZIKV) is responsible for congenital microcephaly. Meertens et al. show that the Axl receptor is expressed in microglia and astrocytes in the human developing brain. They also highlight the dual role of Axl during infection, which promotes viral entry and dampens innate immune responses in glial cells.
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