1995 Fiscal Year Final Research Report Summary
An teratological experimental study of brain abnormalities induced by intrauterine infection with cytomegalovirus
| Project/Area Number |
06671173
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Hamamatsu University School of medicine |
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Principal Investigator |
TSUTSUI Yoshihito Hamamatsu University School of Medicine, Professor, 医学部, 教授 (50073135)
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| Co-Investigator(Kenkyū-buntansha) |
MASAGO Sonomi (AIBA Sono) Hamamatsu Unversity Hospital, Senior resident, 医学部付属病院, 医員
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| Project Period (FY) |
1994 – 1995
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| Keywords | cytomegalovirus / viral teratology / brain anomalies / neuronal migration / brain development |
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| Research Abstract |
The susceptibility of mice at different developmental stages to a relatively low titer of cell culuture-passeged murine cytomegalovirus (MCMV) infection was compared in terms of the urinary excretion of MCMV examined by plaque assay and in terms of the distribution of viral infection, determned by immunohistochemistry, using antibodies specific to the early nuclear antigenof MCMV.Viral infection on day 8.5 of getation (E8.5) into the conceptus and intraperitoneal infection on day 15.5 of gestation (E15.5), postnatal day 2 (P2), postnatal day 11 (P11), and 30 days after birth (P30), respectively, were performed. Embryonal and perinatal mice were more susceptible to MCMV in terms of urinary excretion of the virus and the presence of viral antigen-positive cells in the brain, lungs, and kidneys. In the embryonal and perinatal infection, the viral antigen-positive cells in the neurons of the cerebral cortex and hippocampus were retained late after birth, even though the positive cells in the lungs and kidneys had disappeared. In the mice infected on E8.5, small clusters of viral antigen-positive cells were detected only in the cortex and hippo-campus late after birth, without the urinary excretion of virus. These results suggest that when mice are infected with MCMV at the embryonal and perinatal stages, elimination of the infected neurons is delayd compared with that of the other cells in the lungs and kidneys. These findings provide a model for the anyalysis of pathogenesis of the subclinical congenital CMV infection that manifested clinically late after birth in humans as brain disorders.
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