Search

The present study was carried out to clarify the mode of encephalomyocarditis (EMC) virus infection in pregnant mice. Pregnant BALB/c mice were intraperitoneally inoculated with the D variant of EMC virus (EMC-D) (5 x 10(2) PFU/mouse) on 11 days of gestation and killed at 1, 3, and 5 days post-inoculation (DPI). The virus titer (dam's serum, placenta, and fetus), histopathology (fetus, placenta, and uterus), distribution of viral RNA (fetus, placenta and uterus), and ultrastructure (fetal heart and placenta) were examined. No deaths occurred to fetuses at 1 DPI but almost all fetuses died at 5 DPI. The virus titers of dam's serum and placenta were elevated at 1 DPI, peaked at 3 DPI, and the former was not detected at 5 DPI. The virus titer of fetus was first elevated at 3 DPI and the level was lower than those of others. Histopathological changes and signals of viral RNAs detected by in situ hybridization (ISH) were observed in the spongiotrophoblast layer of placenta and in the fetal myocardium and liver at 3 DPI. The uterus was free from lesions and signals of viral RNA. Ultrastructural changes developed in trophoblast cells and giant cells in the spongiotrophoblast layer at and after 1 DPI and in fetal myocardial cells at 3 DPI. In the cytoplasm of trophoblast cells and giant cells, aggregations of virus-like particles 20-30 nm in diameter were observed in crystalline array. These results suggest that trophoblast cells and giant cells in the spongiotrophoblast layer are the main target of EMC virus in the placenta and that placental damage as well as the direct effect of virus to fetuses may be a cause of fetal death.

Pregnant mice of the BALB/c CrSlc strain were experimentally infected with the D variant of encephalomyocarditis virus (EMC-D, 5 x 10(2) PFU/head) on three different gestational days (GD). Mice were intraperitoneally inoculated with EMC-D on 11, 13 and 15 GD and sacrificed 3 days post inoculation. There was no significant difference in the fetal mortality among all inoculation groups. Placenta showed higher virus titer than fetus and dam's serum in all inoculation groups, and the virus titer of the fetus was lowest in the 15GD group. Histopathological changes and signals of viral RNAs detected by in situ hybridization were observed almost restricted to the spongiotrophoblast layer of the placenta in all inoculation groups, and the signals were strongest in the 11GD group. In the fetus of the11GD group, signals of viral RNAs were also seen in myocardium and hepatocytes. Ultrastructurally, intracytoplasmic aggregations of virus-like particles in crystalline array were observed in trophoblast cells and giant cells in the spongiotrophoblast layer in all inoculation groups.