| Literature DB >> 28314593 |
Chunfeng Li1, Yong-Qiang Deng2, Shuo Wang3, Feng Ma4, Roghiyh Aliyari5, Xing-Yao Huang2, Na-Na Zhang6, Momoko Watanabe7, Hao-Long Dong2, Ping Liu8, Xiao-Feng Li2, Qing Ye2, Min Tian9, Shuai Hong3, Junwan Fan3, Hui Zhao2, Lili Li8, Neda Vishlaghi7, Jessie E Buth7, Connie Au5, Ying Liu8, Ning Lu8, Peishuang Du8, F Xiao-Feng Qin10, Bo Zhang11, Danyang Gong12, Xinghong Dai12, Ren Sun12, Bennett G Novitch13, Zhiheng Xu14, Cheng-Feng Qin15, Genhong Cheng16.
Abstract
Zika virus (ZIKV) has become a public health threat due to its global transmission and link to severe congenital disorders. The host immune responses to ZIKV infection have not been fully elucidated, and effective therapeutics are not currently available. Herein, we demonstrated that cholesterol-25-hydroxylase (CH25H) was induced in response to ZIKV infection and that its enzymatic product, 25-hydroxycholesterol (25HC), was a critical mediator of host protection against ZIKV. Synthetic 25HC addition inhibited ZIKV infection in vitro by blocking viral entry, and treatment with 25HC reduced viremia and conferred protection against ZIKV in mice and rhesus macaques. 25HC suppressed ZIKV infection and reduced tissue damage in human cortical organoids and the embryonic brain of the ZIKV-induced mouse microcephaly model. Our findings highlight the protective role of CH25H during ZIKV infection and the potential use of 25HC as a natural antiviral agent to combat ZIKV infection and prevent ZIKV-associated outcomes, such as microcephaly.Entities:
Keywords: 25HC; CH25H; ZIKV; antiviral immunity; microcephaly
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Year: 2017 PMID： 28314593 PMCID： PMC5957489 DOI： 10.1016/j.immuni.2017.02.012
Source DB: PubMed Journal: Immunity ISSN： 1074-7613 Impact factor: 31.745