摘要Zika virus(ZIKV)infection can cause severe neurological diseases including neonatal microcephaly and Guillain-Barre syndrome.Long noncoding RNAs(lncRNAs)are the by-products of the transcription process,which are considered to affect viral infection.However,it remains largely unexplored whether host lncRNAs play a role in ZIKV infection.Here,we identified a group of human lncRNAs that were up-regulated upon ZIKV infection and were dependent on the type Ⅰ interferon(IFN)signaling.Overexpression of lncRNA ZAP-IT1 leads to an impairment of ZIKV infection.Correspondently,deficiency of ZAP-IT1 led to an enhancement of ZIKV infection.We further confirmed that ZAP-IT1,an intronic lncRNA with total 551 nt in length,is mainly located in the nuclear upon ZIKV infection.Knockout of ZAP-IT1 also led to the increase of dengue virus(DENV),Japanese encephalitis virus(JEV),or vesicular stomatitis virus(VSV)infection.Mechanically,we found that the antiviral effect of ZAP-IT1 was independent of the type Ⅰ IFN signaling pathway.Therefore,our data unveiled that host lncRNA ZAP-IT1 induced by the type Ⅰ IFN signaling,showed robust restriction on ZIKV infection,and even on DENV,JEV,and VSV infection,which may benefit the development of antiviral therapeutics.