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Mild SARS-CoV-2 maternal infection in mice induces transient offspring neurodevelopmental aberrance

ABSTRACT: Maternal viral infection during pregnancy has been identified as a risk factor for psychiatric disorders and neurodevelopmental abnormalities in offspring. With cumulative SARS-CoV-2 infections now numbering in the hundreds of millions globally, there is a need to evaluate the effects of maternal SARS-CoV-2 infection on offspring brain development and behavior. We developed a mouse model of mild SARS-CoV-2 infection during pregnancy, where SARS-CoV-2 infection is restricted to the respiratory tract. These mice did not exhibit weight loss despite detectable local and systemic immune responses, including placental inflammation. Characterization of the offspring cerebral cortex revealed transient transcriptomic changes at post-natal day 5 (P5), but no gross alterations in the cytoarchitecture, synaptic density, or microglia abundance. Moreover, we did not detect any significant changes in open field nor novel object recognition tests in P50 offspring born to SARS-CoV-2-infected dams. These results suggest that mild SARS-CoV-2 infection induces transient perturbations to offspring brain development but does not appear to result in long-lasting structural or behavioral deficits.

ORGANISM(S): Mus musculus

PROVIDER: GSE317803 | GEO | 2026/01/30

REPOSITORIES: GEO

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Project description:<p>The endemic of SARS-CoV-2 underscores the imperative to elucidate its effects on pregnancy, particularly regarding the potential for vertical transmission and its influence on the early maternal-fetal interface, which remain insufficiently defined. To address this, we performed an extensive cohort study involving 761 pregnant women who voluntarily terminated the pregnancy during the first trimester. Analyses conducted using qRT-PCR, fluorescence in situ hybridization, and indirect immunofluorescence assay revealed minimal indications of SARS-CoV-2 infection within chorionic and decidual tissues. Although both tissues exhibited substantial expression of the viral entry receptors ACE2 and TMPRSS2, single-cell RNA sequencing analysis identified no cell populations with significant co-expression of these receptors. The restricted co-expression of viral entry receptors provides a mechanistic explanation for the rare occurrence of direct viral infection in placental tissues. The maternal systemic inflammatory response was notably attenuated relative to the classical cytokine storm, with only IL-31, IL-5, and GRO-α exhibiting elevated levels during acute infection. Furthermore, elevated IgG titers were inversely correlated with tumor necrosis TNF-β concentrations, suggesting a protective immunomodulatory function of IgG antibodies. Conversely, both bulk and single-cell transcriptomic analyses revealed pronounced, cell type-specific antiviral and immune responses within the placental microenvironment. A pervasive interferon-stimulated gene signature was identified, accompanied by emergence of M2-like macrophages with diminished antigen presentation capacity in convalescence. Importantly, maternal SARS-CoV-2 infection disrupted intercellular communication networks, notably impairing WNT and TGF-β signaling pathways to trophoblasts, thereby altering their differentiation trajectories. In summary, within this large first-trimester cohort, evidence for vertical transmission of SARS-CoV-2 was minimal. Nonetheless, infection substantially perturbs the placental immune milieu and trophoblast dynamics, which may adversely affect pregnancy outcomes.</p>

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Mild SARS-CoV-2 maternal infection in mice induces transient offspring neurodevelopmental aberrance

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