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Updated: Jun 8, 2026
Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates
Published on: July 6, 2013
Effect of cytomegalovirus infection on temporal lobe development in utero: quantitative MRI studies
Chen Hoffmann1, Rachel Grossman, Inna Bokov
1Radiology Department, Chaim Sheba Medical Center, Tel Hashomer, Israel.
Abstract:
Several environmental factors, including viral infections during fetal development, are known to increase the risk of schizophrenia. Cytomegalovirus (CMV) is the main cause of viral congenital infection. Since changes in temporal lobe structures are a consistent finding in imaging studies of adult schizophrenics, we investigated possible derangement in temporal lobe development in CMV infected fetuses. Abdominal MRI (1.5 T) was performed using a single-shot fast spin echo T2-weighted sequence. MRI volumetry was employed to measure brain and temporal lobe size in 27 CMV infected fetuses and 52 gestational age matched controls in utero. The ratio of temporal lobe to whole brain was computed for each fetus and group comparisons were performed using Student's t-test or ANOVA. Temporal lobe volumes, normalized to whole brain and co-varied with gestational age; were significantly smaller in fetuses infected with CMV compared to uninfected fetuses. (Infected group mean ± SEM: 0.086 ± 0.006, controls: 0.113 ± 0.003, p<0.0001). Infection during the 1st and 2nd trimester had a more pronounced effect than infection during the 3rd trimester. Infected fetuses with no MRI findings had significantly lower temporal lobe/whole brain ratios than controls (0.092 ± 0.008, p<0.01, N=11) and the lowest ratios were observed in fetuses with overt findings such as cysts or gray matter heterotopy (0.067 ± 0.015). These results demonstrate the ability of quantitative fetal brain MRI to detect previously unreported, specific deficits in brain development in CMV infected fetuses, which, in conjunction with other genetic and environmental factors, may contribute to the risk of developing schizophrenia later in life.
Insights
Congenital cytomegalovirus (CMV) infection in fetuses is linked to smaller temporal lobe brain development. This prenatal brain abnormality may increase schizophrenia risk later in life.
Area of Science:
- Neuroscience
- Developmental Biology
- Radiology
Background:
- Environmental factors, including prenatal viral infections, are associated with an increased risk of schizophrenia.
- Cytomegalovirus (CMV) is a primary cause of congenital viral infections.
- Schizophrenia is consistently linked to temporal lobe structural changes in adults.
Purpose of the Study:
- To investigate potential temporal lobe developmental abnormalities in fetuses infected with cytomegalovirus (CMV).
- To assess the impact of prenatal CMV infection on fetal brain development using advanced imaging techniques.
Main Methods:
- Quantitative fetal brain MRI (1.5 T, T2-weighted sequence) was used to measure brain and temporal lobe volumes in 27 CMV-infected fetuses and 52 controls.
- MRI volumetry was employed to calculate the ratio of temporal lobe to whole brain volume.
- Statistical analysis (Student's t-test, ANOVA) was performed to compare groups, controlling for gestational age.
Main Results:
- Fetuses infected with CMV exhibited significantly smaller temporal lobe volumes relative to whole brain size compared to uninfected controls (p<0.0001).
- First and second-trimester CMV infections showed a more significant impact on temporal lobe development than third-trimester infections.
- Even in infected fetuses without overt MRI abnormalities, temporal lobe/whole brain ratios were reduced, with the lowest ratios observed in those with cysts or gray matter heterotopia.
Conclusions:
- Quantitative fetal MRI can detect specific, previously unreported deficits in brain development caused by prenatal CMV infection.
- These CMV-induced developmental deficits in the temporal lobe may represent a biological pathway contributing to schizophrenia risk.
- Prenatal CMV infection is a significant risk factor for neurodevelopmental alterations potentially linked to schizophrenia.
