Zika virus suppresses maturation of human dendritic cells

• Published in: The Journal of immunology (1950) 2020-05, Vol.204 (1_Supplement), p.248-248.11
• Main Authors: Wang, Ying-Ting, Branche, Emilie, Viramontes, Karla M., Cuevas, Joan Valls, Carlin, Aaron F., Shresta, Sujan
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.204.Supp.248.11

Zika virus (ZIKV) belongs to the genus Flavivirus, which includes several medically relevant viruses, including dengue, yellow fever and Japanese encephalitis viruses. ZIKV causes congenital Zika syndrome in neonates and Guillain-Barré syndrome in adults, and has emerged as a major public health problem worldwide. Dendritic cells (DCs) serve as the major cellular hosts of ZIKV, and T cell responses to flaviviruses may play a dual role in protection and pathogenesis. To decipher the precise interactions between DCs and ZIKV, we profiled the transcriptomic features of ZIKV-infected DCs versus uninfected bystander DCs in primary human blood monocyte-derived DC cultures. RNA sequencing data revealed that the expression of genes related to antigen processing/presentation pathways was reduced in ZIKV-infected DCs relative to uninfected bystander DCs that were exposed to the same environmental stimuli as ZIKV-infected DCs. Flow cytometric analysis of ZIKV-infected DCs for the expression of key DC maturation markers confirmed the RNA sequencing data. Thus, ZIKV hinders DC maturation, suggesting that ZIKV may modulate T cell responses by directly manipulating DC functions. Studies are in progress to determine how ZIKV inhibits DC maturation and influences T cell responses. Results of these studies will provide key insights towards the development of safe and effective vaccines against ZIKV and related flaviviruses.