Full Name
Aïssatou Aïcha Sow
Job Title
PhD Candidate
Armand-Frappier Santé Biotechnologie Research Center, Institut National de la Recherche Scientifique
City (Work Address)
State/Province/County (Work Address)
Speaker Bio
Aïssatou Aïcha Sow is a PhD candidate in molecular virology at Armand-Frappier Santé Biotechnologie Research Center (Institut national de la recherche scientifique, Quebec). She is part of Dr Laurent Chatel-Chaix’ team, and her project focuses on developing a novel in vivo model to study Zika virus pathogenesis. Her research is supported by Brain Canada Foundation. She is also the recipient of two excellence scholarships (Center of Excellence in Research on Orphan Diseases – Fondation Courtois and Armand-Frappier Foundation). Aïcha holds a B.Sc in Biomedical Sciences, a M.Sc in Biochemistry, and a Graduate Certificate in Global Health (Université de Montréal).
Aside from her research work, social involvement is a major part of her extra-curricular life. Over the past 18 months, she has served on the Canadian Society for Virology’s executive committee as the trainee representative. Aïcha has also been involved in science outreach. Her commitment to the values of Equity, Diversity, and Inclusion earned her a spot on the list of ‘Those who made the gender in 2020’ by the Gender in Geopolitics Institute.
Abstract Title
A novel zebrafish-based in vivo model of Zika virus infection unveils NS4A as a key viral determinant of neuropathogenesis
Abstract Summary
Infection of pregnant women by Zika virus (ZIKV) can cause in newborns neurodevelopmental defects, which viral determinants are poorly defined. Murine models studying ZIKV neurovirulence have several limitations in terms of cost, time, ethics, cell imaging, and genetic manipulation. Thus, alternative animal models to study the early development of the ZIKV-infected brain are required.
Zebrafish is a powerful tool for studying human neurological and infectious diseases. Optically transparent, it is ideal for imaging labelled specific neural cell populations. Considering this, we aimed to develop a zebrafish in vivo model of ZIKV infection to study viral neuropathogenesis.

Eighty percent of zebrafish larvae infected with ZIKV exhibited developmental defects. TUNEL assays showed an increased apoptosis in the brain following ZIKV infection. This correlated with a decrease in head size and in neural progenitor cell abundance, and drastic mobility impairments. Importantly, these defects were reversed when the larvae were treated with the flaviviral inhibitor NITD008, which decreased viral load more than 150-fold, unambiguously demonstrating that ZIKV replicates in zebrafish. Whole animal immunostaining revealed infection foci in the hindbrain and in the spinal cord, supporting that ZIKV replicates in the central nervous system. Furthermore, expression of viral protein NS4A alone recapitulated morphological defects, demonstrating that NS4A is a key determinant in ZIKV neurovirulence.

Overall, our data unveil the zebrafish larva as a model for ZIKV infection with neurological phenotypes comparable to those in humans. This model will enable better understanding of host determinants required for ZIKV neuropathogenesis given its flexibility for genetic manipulations.
Aïssatou Aïcha Sow