VIP decreases zika virus propagation in first-trimester cytotrophoblast cells and restores cell migration. D Kafer, A Marquez, D Paparini, F Merech, B Lara, V Hauk, R Ramhorst1, C Pérez Leirós, C Garcia, D Vota.

D KAFER, A MARQUEZ, D PAPARINI, F MERECH, B LARA, V HAUK, R RAMHORST, C PÉREZ LEIRÓS, C GARCIA, D VOTA.

virtual

Congreso; Reunión Anual Conjunta SAIC-SAI-SAFIS; 2021

SAIc-SAI-SAFIS

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 glu-cose 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 demon-strated 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-tri-mester human Tb cells and explore the potential antiviral effect of the endogenous polypeptide VIP. Material and Methods: We infect-ed first-trimester Tb-derived cell line Swan-71 with an isolated local ZIKV strain in the presence/absence of VIP. Tb migration was as-sessed 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 expres-sion. However, a significantly higher increment in the anti-apoptot-ic factor BCL-2 was detected (2.5-fold increase of BCL-2 vs BAK p