VIP DECREASES ZIKA VIRUS PROPAGATION IN FIRST-TRIMESTER CYTOTROPHOBLAST CELLS AND RESTORES CELL MIGRATION

AGOSTINA MÁRQUEZ; BRENDA LARA; CLAUDIA PÉREZ LEIROS; DANIEL PAPARINI; VANESA HAUK; CYBELE GARCÍA; DIEGO KAFER; FÁTIMA MERECH; ROSANNA RAMHORST; DAIANA VOTA

Ciudad Autónoma de Buenos Aires

Congreso; REUNIÓN DE SOCIEDADES DE BIOCIENCIAS 2021 SAIC - SAI - AAFE - NANOMED-ar; 2021

SAI-SAIC-AAFE-Nanomed

Objective: Zika virus (ZIKV) infection during pregnancy is associated to an increased risk of fetal growth impairment and altered central nervous system development. We have previously demonstrated that ZIKV impaired trophoblast cell (Tb) migration, increased glucose uptake and decreased the brain derived neurotrophic factor (BDNF) expression. Up to date there is no treatment or vaccines to ameliorate the observed fetal growth defects. We previously demonstrated that the vasoactive intestinal peptide (VIP) not only favors immune homeostasis maintenance but modulates trophoblast cell invasion and metabolism at early pregnancy. Our aim is to elucidate the metabolism and signaling pathways altered by ZIKV in first-trimester human Tb cells and explore the potential antiviral effect of the endogenous polypeptide VIP. Material and Methods: We infected first-trimester Tb-derived cell line Swan-71 with an isolated local ZIKV strain in the presence/absence of VIP. Tb migration was assessed in wound healing assays, RNA expression by RT- qPCR and viral production by the lysis plaque assay. Results: ZIKV induces an increase of NFKB and the proapoptotic factor BAK mRNA expression. However, a significantly higher increment in the anti-apoptotic factor BCL-2 was detected (2.5-fold increase of BCL-2 vs BAK p