ArticleViruses2025
Mild Zika Virus Infection in Mice Without Motor Impairments Induces Working Memory Deficits, Anxiety-like Behaviors, and Dysregulation of Immunity and Synaptic Vesicle Pathways.
Article in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Alterations in the Components of the GABA-Glutamate System During ZIKV Infection: A Neuroscience Approach.International journal of molecular sciences · 2026Article
- Ebola's hidden front: Neurological involvement and pathogenesis.PLoS pathogens · 2025Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe Zika virus (ZIKV) is an arbovirus linked to "Congenital Zika Syndrome" and a range of neurodevelopmental disorders (NDDs), with microcephaly as the most severe manifestation. Milder NDDs, such as autism spectrum disorders and delays in neuropsychomotor and language development, often go unnoticed in neonates, resulting in long-term social and academic difficulties. Murine models of ZIKV infection can be used to mimic part of the spectrum of motor and cognitive deficits observed in humans. These can be evaluated through behavioral tests, enabling comparison with gene expression profiles and aiding in the characterization of ZIKV-induced NDDs.
objectivesThis study aimed to identify genes associated with behavioral changes following a subtle ZIKV infection in juvenile BALB/c mice.
methodsNeonatal mice were subcutaneously inoculated with ZIKV (MH544701.2) on postnatal day 1 (DPN) at a dose of 6.8 × 10
resultsA ZIKV infection model was successfully established, enabling brain infection while allowing survival beyond 30 DPI. The infection induced mild cognitive behavioral changes, though motor and motivational functions remained unaffected. These cognitive changes were linked to the functional repression of synaptic vesicles and alterations in neuronal structure, suggesting potential disruptions in neuronal plasticity.
conclusionsModerate ZIKV infection with circulating strains from the 2016 epidemic may cause dysregulation of genes related to immune response, alterations in cytoskeletal organization, and modifications in cellular transport mediated by vesicles. Despite viral control, neurocognitive effects persisted, including memory deficits and anxiety-like behaviors, highlighting the long-term neurological consequences of ZIKV infection in models that show no apparent malformations.
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