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© Research
Publication : Frontiers in Immunology

Zika Virus Inhibits IFN-α Response by Human Plasmacytoid Dendritic Cells and Induces NS1-Dependent Triggering of CD303 (BDCA-2) Signaling

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Frontiers in Immunology - 28 Oct 2020

Bos Sandra, Poirier-Beaudouin Béatrice, Seffer Valérie, Manich Maria, Mardi Cartini, Desprès Pesprès, Gadea Gilles, Gougeon Marie-Lise

Link to Pubmed [PMID] – 33193389

Link to DOI – 10.3389/fimmu.2020.582061

Front Immunol. 2020 Oct 28;11:582061

Zika virus (ZIKV) dramatically emerged in French Polynesia and subsequently in the Americas where it has been associated with severe neurological complications in adults and newborns, respectively. Although plasmacytoid dendritic cells (pDCs) are a key sensor of viral infection and are critical for initiating an antiviral response, little is known about the impact of ZIKV infection on pDCs. Here, we investigated the susceptibility of human pDCs to infection with multiple strains of ZIKV and further investigated the impact of infection on pDCs functions. We observed that pDCs were refractory to cell-free ZIKV virions but were effectively infected when co-cultured with ZIKV-infected cells. However, exposure of pDCs to ZIKV-infected cells resulted in limited maturation/activation with significant down regulation of CD303 expression, a severe impairment of inflammatory cytokine production, and an inability to mount an IFN-α response. We show that ZIKV developed a strategy to inhibit the IFN-α response in primary human pDCs likely mediated through NS1-dependent CD303 signaling, thus suggesting a new mechanism of immune evasion.

https://www.frontiersin.org/articles/10.3389/fimmu.2020.582061/full