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Zika virus infection preferentially counterbalances human peripheral monocyte and/or NK-cell activity

By Fok Moon Lum, David Lee, Tze-Kwang Chua, Jeslin JL Tan, Cheryl YP Lee, Xuan Liu, Yongxiang Fang, Bernett Lee, Wearn-Xin Yee, Natasha Y Rickett, Po-Ying Chia, Vanessa Lim, Yee-Sin Leo, David Matthews, Julian A Hiscox, Lisa FP Ng

Posted 25 Nov 2017
bioRxiv DOI: 10.1101/225102 (published DOI: 10.1128/mspheredirect.00120-18)

Zika virus (ZIKV) has re-emerged in the population and caused unprecedented global outbreaks. Here, the transcriptomic consequences of ZIKV infection were studied systematically firstly in human peripheral blood CD14+ monocytes and monocyte-derived macrophages with high density RNA-sequencing. Analyses of the ZIKV genome revealed that the virus underwent genetic diversification and differential mRNA abundance was found in host cells during infection. Notably, there was a significant change in the cellular response with crosstalk between monocytes and natural killer (NK) cells as one of the highly identified pathway. Immune-phenotyping of peripheral blood from ZIKV-infected patients further confirmed the activation of NK cells during acute infection. ZIKV infection in peripheral blood cells isolated from healthy donors led to the induction of IFNγ and CD107a — two key markers of NK-cell function. Depletion of CD14+ monocytes from peripheral blood resulted in a reduction of these markers and reduced priming of NK cells during infection. This was complemented by the immunoproteomic changes observed. Mechanistically, ZIKV infection preferentially counterbalances monocyte and/or NK-cell activity, with implications for targeted cytokine immunotherapies.

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