INHIBITION OF THE TYPE I INTERFERON ANTIVIRAL RESPONSE BY ZIKA VIRUS NS4B PROTEIN

SARRATEA, MARÍA B.; SANCHEZ-ALBERTI, ANDRÉS; BIVONA, AUGUSTO E.; ANTONOGLOU, MARÍA B.; NOLI TRUANT, SOFÍA; FERNÁNDEZ LYNCH, MARÍA J.; ROMASANTA, PABLO; FERNÁNDEZ, MARISA M.; MALCHIODI, EMILIO L.

CABA

Congreso; REUNIÓN CONJUNTA DE SOCIEDADES DE BIOCIENCIAS 2017; 2017

Sociedad Argentina de Inmunología

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