ArticleFrontiers in cellular and infection microbiology2025
Neurogenesis decreases in the offspring of mothers infected with influenza A virus.
Article in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Influenza virus infection during pregnancy: a review of risk factors, pathogenic mechanisms, and prevention strategies.Frontiers in immunology · 2026Review
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15 authors.
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Abstract
Introduction: 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. Methods: Mice were infected with the mouse-adapted influenza virus strain A/WSN/33 (H1N1) or A/California/07/09 (H1N1)pdm09 in a sublethal dose 14 days after pregnancy manifestation. After birth, several pups were sacrificed, brains and hippocampi were isolated and used for RT-qPCR (the expression of IL-1β, iNOS, IFNG, IL-6, TNFa was assessed), immunohistochemistry and Western blot for markers of neural progenitors (Sox2, Sox11), mature neurons (NeuN), microglia (Iba1), and astrocytes (GFAP). Within 2 weeks after birth, the mortality and body weight dynamics change were monitored in the remaining pups. Results and discussion: Findings reveal that maternal infection with H1N1wsn 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.
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