Zika but not Dengue virus infection limits NF-κB activity in human monocyte-derived dendritic cells and suppresses their ability to activate T cells

Ying-Ting Wang, Emilie Branche, Jialei Xie, Rachel E. McMillan, Fernanda Ana-Sosa-Batiz, Hsueh-Han Lu, Qin Hui Li, Alex E. Clark, Joan M. Valls Cuevas, Karla M. Viramontes, Aaron F. Garretson, Rúbens Prince Santos Alves, Sven Heinz, Christopher Benner, Aaron F. Carlin () and Sujan Shresta ()
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Ying-Ting Wang: La Jolla Institute for Immunology
Emilie Branche: La Jolla Institute for Immunology
Jialei Xie: San Diego
Rachel E. McMillan: San Diego
Fernanda Ana-Sosa-Batiz: La Jolla Institute for Immunology
Hsueh-Han Lu: La Jolla Institute for Immunology
Qin Hui Li: La Jolla Institute for Immunology
Alex E. Clark: San Diego
Joan M. Valls Cuevas: La Jolla Institute for Immunology
Karla M. Viramontes: La Jolla Institute for Immunology
Aaron F. Garretson: San Diego
Rúbens Prince Santos Alves: La Jolla Institute for Immunology
Sven Heinz: San Diego
Christopher Benner: San Diego
Aaron F. Carlin: San Diego
Sujan Shresta: La Jolla Institute for Immunology

Nature Communications, 2025, vol. 16, issue 1, 1-14

Abstract: Abstract Understanding flavivirus immunity is critical for the development of pan-flavivirus vaccines. Dendritic cells (DC) coordinate antiviral innate and adaptive immune responses, and they can be targeted by flaviviruses as a mechanism of immune evasion. Using an unbiased genome-wide approach designed to specifically identify flavivirus-modulated pathways, we found that, while dengue virus (DENV) robustly activates DCs, Zika virus (ZIKV) causes minimal activation of genes involved in DC activation, maturation, and antigen presentation, reducing cytokine secretion and the stimulation of allogeneic and peptide-specific T cell responses. Mechanistically, ZIKV inhibits DC maturation by suppressing NF-κB p65 recruitment and the subsequent transcription of proinflammatory and DC maturation-related genes. Thus, we identify a divergence in the effects of ZIKV and DENV on the host T cell response, highlighting the need to factor such differences into the design of anti-flavivirus vaccines.

Date: 2025
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DOI: 10.1038/s41467-025-57977-2

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