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AXL promotes Zika virus infection in astrocytes by antagonizing type I interferon signalling.

Abstract：

:Zika virus (ZIKV) is associated with neonatal microcephaly and Guillain-Barré syndrome1,2. While progress has been made in understanding the causal link between ZIKV infection and microcephaly3-9, the life cycle and pathogenesis of ZIKV are less well understood. In particular, there are conflicting reports on the role of AXL, a TAM family kinase receptor that was initially described as the entry receptor for ZIKV10-22. Here, we show that while genetic ablation of AXL protected primary human astrocytes and astrocytoma cell lines from ZIKV infection, AXL knockout did not block the entry of ZIKV. We found, instead, that the presence of AXL attenuated the ZIKV-induced activation of type I interferon (IFN) signalling genes, including several type I IFNs and IFN-stimulating genes. Knocking out type I IFN receptor α chain (IFNAR1) restored the vulnerability of AXL knockout astrocytes to ZIKV infection. Further experiments suggested that AXL regulates the expression of SOCS1, a known type I IFN signalling suppressor, in a STAT1/STAT2-dependent manner. Collectively, our results demonstrate that AXL is unlikely to function as an entry receptor for ZIKV and may instead promote ZIKV infection in human astrocytes by antagonizing type I IFN signalling.

journal_name

Nat Microbiol

journal_title

Nature microbiology

authors

Chen J,Yang YF,Yang Y,Zou P,Chen J,He Y,Shui SL,Cui YR,Bai R,Liang YJ,Hu Y,Jiang B,Lu L,Zhang X,Liu J,Xu J

doi

10.1038/s41564-017-0092-4

subject

Has Abstract

pub_date

2018-03-01 00:00:00

pages

302-309

issue

3

issn

2058-5276

pii

10.1038/s41564-017-0092-4

journal_volume

3

pub_type

杂志文章

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