Viral infection, inflammation and schizophrenia
Open accessAbstract
Schizophrenia is a severe neurodevelopmental disorder with genetic and environmental etiologies. Prenatal viral/bacterial infections and inflammation play major roles in the genesis of schizophrenia. In this review, we describe a viral model of schizophrenia tested in mice whereby the offspring of mice prenatally infected with influenza at E7, E9, E16, and E18 show significant gene, protein, and brain structural abnormalities postnatally. Similarly, we describe data on rodents exposed to bacterial infection or injected with a synthetic viral mimic (PolyI:C) also demonstrating brain structural and behavioral abnormalities. Moreover, human serologic data has been indispensible in supporting the viral theory of schizophrenia. Individuals born seropositive for bacterial and viral agents are at a significantly elevated risk of developing schizophrenia. While the specific mechanisms of prenatal viral/bacterial infections and brain disorder are unclear, recent findings suggest that the maternal inflammatory response may be associated with fetal brain injury. Preventive and therapeutic treatment options are also proposed. This review presents data related to epidemiology, human serology, and experimental animal models which support the viral model of schizophrenia.
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PVI deficits in the DISC1-dominant negative transgenic mouse are exacerbated by a neonatal PolyI:C challenge.
“Furthermore, PVI deficits in the DISC1-dominant negative transgenic mouse are exacerbated by a neonatal Polyl:C challenge 91 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [91]
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- Authors
- Kneeland, R. E., & Fatemi, S. H.
- Affiliations
- University of Minnesota (US)
- Corresponding author
- Fatemi, S. Hossein
- ORCID
- Fatemi, S. Hossein
- Venue
- Progress in Neuro-Psychopharmacology and Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2013-04
- Volume
- 42
- Pages
- 35-48
- ISSN
- 0278-5846 (ISSN-L)
- PMC
- PMC3408569
- OpenAlex
- W2002231678
- Cited by
- 152
- References
- 241
- Citations by year
- 2025: 8 · 2024: 11 · 2023: 6 · 2022: 12 · 2021: 11 · 2020: 16 · 2019: 7 · 2018: 11 · 2017: 10 · 2016: 15 · 2015: 13 · 2014: 14 · 2013: 7 · 2012: 11
- FWCI
- 0.93
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Progress in Neuro-Psychopharmacology and Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD046589)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- schizophrenia, prenatal viral infection, maternal inflammation, influenza, mouse model of schizophrenia, poly(I:C), structural brain abnormalities, behavioral abnormalities, serological markers, neurodevelopmental disorders, fetal brain injury, prophylaxis
- MeSH terms
- Animals, Encephalitis, Female, Humans, Pregnancy, Prenatal Exposure Delayed Effects, Schizophrenia, Central Nervous System Viral Diseases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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