ZIKA VIRUS NS4b PROTEIN IMPAIRS TRANSLOCATION OF INTERFERON REGULATORY FACTOR 3 TO THE NUCLEUS

NOLI TRUANT SOFIA; IANNANTUONO LÓPEZ, LAURA; FERNÁNDEZ MARISA MARIEL; ANTONOGLOU, BELÉN; REDOLFI, DANIELA; SANCHEZ ALBERTI, ANDRÉS; SARRATEA, BELÉN; BIVONA, AUGUSTO; TABOADA, GUILLERMO; EMILIO L. MALCHIODI

Mar del Plata, Buenos Aires.

Congreso; Reunión Conjunta de la Sociedad Argentina de Investigación Clínica (SAIC), la Sociedad Argentina de Inmunología (SAI) y la Sociedad Argentina de Fisiología (SAFIS).; 2018

SAIC-SAI-SAFE

Type I interferons (IFN I) play an essential role in innate immunity against viral infections. When a cell is infected with a virus, microbial components can be sensed by intracellular pattern recognition receptors, activating interferon regulatory factor 3 (IRF3) and inducing the production of IFN I. However, many pathogens have evolved strategies to evade immune sensing favoring their survival. Among them, flaviviral non-structural proteins, needed for viral replication, are involved in host immune evasion. Here, we aimed to broaden the understanding of the role of Zika virus (ZIKV) NS4b protein in the inhibition of IFN I induction. For this purpose, we performed transfection assays with plasmid encoding recombinant ZIKV NS4b. Using RAW-Lucia ISG cells, an IFN reporter cell-line, we showed that cells with NS4b were able to reduce luciferase signals in a dose dependent manner compared to empty vectors (two-way ANOVA, p