WFRF:(Lu Jun)
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AXL promotes Zika virus infection in astrocytes by antagonizing type I interferon signalling
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- Chen, Jian (author)
- Fudan Univ, Shanghai Publ Hlth Clin Ctr, Sci Res Ctr, Shanghai, Peoples R China.;Fudan Univ, Inst Biomed Sci, Key Lab Med Mol Virol, Minist Educ Hlth,Shanghai Med Coll, Shanghai, Peoples R China.
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- Yang, Yi-feng (author)
- ShanghaiTech Univ, Shanghai Inst Adv Immunochem Studies, Shanghai, Peoples R China.
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- Yang, Yu (author)
- Fudan Univ, Shanghai Publ Hlth Clin Ctr, Sci Res Ctr, Shanghai, Peoples R China.;Fudan Univ, Inst Biomed Sci, Key Lab Med Mol Virol, Minist Educ Hlth,Shanghai Med Coll, Shanghai, Peoples R China.
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- Fudan Univ, Shanghai Publ Hlth Clin Ctr, Sci Res Ctr, Shanghai, Peoples R China;Fudan Univ, Inst Biomed Sci, Key Lab Med Mol Virol, Minist Educ Hlth,Shanghai Med Coll, Shanghai, Peoples R China. ShanghaiTech Univ, Shanghai Inst Adv Immunochem Studies, Shanghai, Peoples R China. (creator_code:org_t)
- 2018-01-29
- 2018
- English.
- In: Nature Microbiology. - : NATURE PUBLISHING GROUP. - 2058-5276. ; 3:3, s. 302-309
- Journal article (peer-reviewed)
Abstract
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- Zika virus (ZIKV) is associated with neonatal microcephaly and Guillain-Barre syndrome(1,2). While progress has been made in understanding the causal link between ZIKV infection and microcephaly(3-9), 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 ZIKV(10-22). 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 alpha 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.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Microbiology in the medical area (hsv//eng)
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- art (subject category)
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- Chen, Jian
- Yang, Yi-feng
- Yang, Yu
- Zou, Peng
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- He, Yongquan
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- Shui, Sai-lan
- Cui, Yan-ru
- Bai, Ru
- Liang, Ya-jun
- Hu, Yunwen
- Jiang, Biao
- Lu, Lu
- Zhang, Xiaoyan
- Liu, Jia
- Xu, Jianqing
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