期刊
VIROLOGICA SINICA
卷 37, 期 6, 页码 904-912出版社
KEAI PUBLISHING LTD
DOI: 10.1016/j.virs.2022.08.003
关键词
Zika virus (ZIKV); Long noncoding RNA (lncRNA); Interferon-stimulated gene (ISG); Restriction factor; Viral replication
类别
资金
- National Natural Science Foundation of China, China [31970887]
- Guangdong Science and Technology Department, China [2018B030337001]
- Guangdong Basic and Applied Basic Foundation [2019A1515011336]
This study reveals that host lncRNA ZAP-IT1 induced by type I IFN signaling has a strong restriction on ZIKV infection, as well as other viral infections, which may benefit the development of antiviral therapeutics.
Zika virus (ZIKV) infection can cause severe neurological diseases including neonatal microcephaly and GuillainBarre 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.
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