| Virus Name | Zika virus |
| Virus Short Name | ZIKV |
| Order | Unassigned |
| Virus Family | Flaviviridae |
| Virus Subfamily | N.A. |
| Genus | Flavivirus |
| Species | Zika virus |
| Host | Human, mammals, mosquitoes and ticks |
| Cell Tropism | N.A. |
| Associated Disease | Zika fever |
| Mode of Transmission | Arthropod bite, mainly mosquitoes |
| VIPR DB link | http://www.viprbrc.org/brc/home.spg?decorator=flavi |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_online_report/positive-sense-rna-viruses/w/flaviviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Flaviviridae |
| Paper Title | AXL promotes Zika virus infection in astrocytes by antagonizing type I interferon signalling |
| Author's Name | Jian Chen, Yi-feng Yang, Yu Yang, Peng Zou, Jun Chen, Yongquan He, Sai-lan Shui, Yan-ru Cui, Ru Bai, Ya-jun Liang, Yunwen Hu, Biao Jiang, Lu Lu, Xiaoyan Zhang, Jia Liu and Jianqing Xu |
| Journal Name | Nature Microbiology |
| Pubmed ID | 29379210 |
| 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 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. |
| Used Model | U-251MG cells |
| DOI | 10.1038/s41564-017-0092-4 |
