ORIGINAL RESEARCH article
Front. Cell. Infect. Microbiol.
Sec. Virus and Host
Neurogenesis decreases in the offspring of mothers infected with influenza A virus
Provisionally accepted
Anastasiya Rakovskaya1
Alexey Lozhkov1,2
Yana Zabrodskaya1,2Valeria Kirenskaya1Olesya Korovina1Angelika Garshinina2Valeria Zryacheva2
Anna Shtro2Ekaterina Pchitskaya1
Olga Vlasova1Ekaterina Elpaeva2
Dmitry Moshkoff1,2,3Maria Salvato4
Ilya Bezprozvanny1
Andrey Vasin1,2,3*- 1Peter the Great St.Petersburg Polytechnic University, Saint Petersburg, Russia
- 2Smorodintsev Research Institute of Influenza, Saint-Petersburg, Russia
- 3The Global Virus Network (GVN) Center of Excellence at Institute of Biomedical Systems and Biotechnology, Saint-Petersburg, Russia
- 4University of Maryland, College Park, United States
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Seasonal influenza virus infection during pregnancy poses significant risks to maternal and fetal health, contributing to adverse neurodevelopmental outcomes in offspring. This study investigates the impact of maternal infection with two highly pathogenic H1N1 influenza A virus (IAV) strains on hippocampal neurogenesis and glial reactivity in neonatal and juvenile mice. Findings reveal that maternal infection with H1N1 A/WSN/33 disrupts early neurogenesis, while infection with H1N1pdm09 induces region-specific reductions in neurogenesis and heightened glial reactivity in 14-day-old offspring. Increased expression of pro-inflammatory cytokines and factors, including IL-1β and iNOS, in neonatal brain tissue suggests that maternal immune activation mediates neurodevelopmental disruptions. Despite reduced Sox2+ and Sox11+ neural progenitor cells, NeuN expression remained stable, implying potential compensatory mechanisms. Elevated astrocyte reactivity in the CA1 and dentate gyrus regions highlights prolonged neuroinflammatory effects. These results underscore the role of maternal influenza-induced immune responses in shaping hippocampal development, with implications for long-term cognitive and behavioral outcomes. Understanding these mechanisms may inform strategies to mitigate neurodevelopmental risks associated with prenatal infections.
Keywords: Influenza Virus, neurodevelopment, Neurogenesis, Neuroinflammation, offspring, Pregnancy
Received: 13 Sep 2025; Accepted: 03 Dec 2025.
Copyright: © 2025 Rakovskaya, Lozhkov, Zabrodskaya, Kirenskaya, Korovina, Garshinina, Zryacheva, Shtro, Pchitskaya, Vlasova, Elpaeva, Moshkoff, Salvato, Bezprozvanny and Vasin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Andrey Vasin
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