| Literature DB >> 29117563 |
Jinling Chen1, Yuejin Liang2, Panpan Yi3, Lanman Xu4, Hal K Hawkins5, Shannan L Rossi6, Lynn Soong7, Jiyang Cai8, Ramkumar Menon9, Jiaren Sun10.
Abstract
Zika virus (ZIKV) infection during pregnancy in humans results in intrauterine growth restriction, spontaneous abortion, and microcephaly. Here, we found that fetus-derived type I interferon (IFN-I) signaling can enhance anti-ZIKV responses and provide clinical benefits to the fetus. Because IFN-λ shares signaling cascades and antiviral functions with IFN-I, we investigated the in vivo effects of IFN-λ in ZIKV-infected pregnant mice. IFN-λ administration during mid-pregnancy reduced ZIKV burden in maternal and fetal organs and alleviated placental injuries and fetal demise. In addition, prophylactic and therapeutic treatment of IFN-λ1 in a human trophoblast line, as well as in primary human amniotic epithelial cells, greatly reduced the ZIKV burden. Our data highlight IFN-λ1 as a potential therapeutic useful for women at risk for congenital Zika disease.Entities:
Keywords: Zika virus; animal model; antiviral; congenital infection; gestational stage; human pregnancy; interferon-λ
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Year: 2017 PMID: 29117563 PMCID: PMC5726784 DOI: 10.1016/j.celrep.2017.10.059
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423