Inhibition of the type I interferon antiviral response by Zika Virus NS4B protein.

SARRATEA, BELÉN; SANCHEZ ALBERTI, ANDRÉS; BIVONA, AUGUSTO; ANTONOGLOU, BELÉN; NOLI TRUANT, SOFIA; FERNÁNDEZ LYNCH MARÍA JULIETA; ROMASANTA, PABLO N.; EMILIO L. MALCHIODI; MARISA M. FERNANDEZ

Ciudad de Buenos Aires

Congreso; Reunión conjunta de Sociedades de Biociencias; 2017

Sociedad Argentina de Investigación Clínica (SAIC), Sociedad Argentina Bioquímica y Biología Molecular (SAIB), Sociedad Argentina Inmunología (SAI), Sociedad Argentina Fisiología (SAFIS), Sociedad Argentina Farmacología Experimental (SAFE), Sociedad Arge

Zika virus (ZIKV) illustrates the importance of flaviviruses as emerging vector-borne human pathogens. The major concern is the association between ZIKV infection and neurological disorders, such as congenital microcephaly and Guillain-Barré syndrome. According to the WHO, there are currently 54 countries with ongoing transmission of the virus, including Argentina. Type I interferons (IFN I) play an important role in innate host defense against viruses. When a cell is infected with a virus, microbial components can be sensed by intracellular receptors and promote IFN I production. However, recent studies have shown that non-structural proteins of dengue virus and other flaviviruses have developed ways to hinder this response. In the present work we aimed to study whether one non-structural protein of ZIKV, NS4b, is able to inhibit IFN I response. For this purpose, we conducted transfection assays using RAW-Lucia ISG cells, an IFN reporter cell-line that secrete Lucia luciferase under ISRE promoter. Results showed that cells transfected with plasmid encoding NS4b were able to inhibit luciferase signals in a dose dependent manner compared to empty vectors (two-way ANOVA, p