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

Fok Moon Lum, David Lee, Tze Kwang Chua, Jeslin J.L. Tan, Cheryl Y.P. Lee, Xuan Liu, Yongxiang Fang, Bernett Lee, Wearn Xin Yee, Natasha Y. Rickett, Po Ying Chia, Vanessa Lim, Yee Sin Leo, David A. Matthews, Julian A. Hiscox, Lisa F.P. Nga*

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)peer-review

23 Citations (Scopus)
391 Downloads (Pure)


Zika virus (ZIKV) has reemerged in the population and caused unprecedented global outbreaks. Here, the transcriptomic consequences of ZIKV infection were studied systematically first 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 cross talk between monocytes and natural killer (NK) cells as one of the highly identified pathways. Immunophenotyping 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 gamma interferon (IFN-γ) 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.

Original languageEnglish
Article numbere00120-18
Issue number2
Publication statusPublished - 28 Mar 2018


  • Immune response
  • Monocytes
  • NK cells
  • RNA-seq
  • Transcriptomes
  • Zika virus


Dive into the research topics of 'Zika virus infection preferentially counterbalances human peripheral monocyte and/or NK cell activity'. Together they form a unique fingerprint.

Cite this