Insights into ZIKV-Mediated Innate Immune Responses in Human Dermal Fibroblasts and Epidermal Keratinocytes

Ji Ae Kim, Rak Kyun Seong, Sang Wook Son, Ok Sarah Shin

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

Abstract

Zika virus (ZIKV) has emerged as a global pathogen causing significant public health concern. ZIKV infections in humans principally occur via mosquito bites. Thus, host skin cells are permissive to ZIKV infection and are the first line of defense against the virus. Here, we examined the role and mechanisms of antiviral skin immunity against ZIKV infection. ZIKV infection (African lineage MR766) in human dermal fibroblasts, human epidermal keratinocytes, and HaCaT keratinocytes resulted in distinct expression changes in RIG-I–like receptors, such as RIG-I and MDA5. Inhibition of RIG-I using small interfering RNA resulted in increased viral gene expression and reduced induction of IFNs and IFN-stimulated genes. Furthermore, ZIKV NS1 directly interacted with RIG-I or MDA5 and down-regulated RIG-I–like receptor–mediated antiviral signaling pathways. Asian lineage ZIKV (PRVABC59) infection also showed a distinct pattern of antiviral immunity in human skin cells, compared with other ZIKV strains. Additionally, ZIKV infections in human neural progenitor cells induced the robust activation of RIG-I–like receptor–mediated signaling, followed by highly enhanced IFN-stimulated gene expression. Our findings provide important insights into ZIKV tropism and subsequent antiviral signaling pathways that regulate ZIKV replication in human dermal fibroblasts and human epidermal keratinocytes.

Original languageEnglish
Pages (from-to)391-399
Number of pages9
JournalJournal of Investigative Dermatology
Volume139
Issue number2
DOIs
Publication statusPublished - 2019 Feb

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology

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