Y. Tsutsui et al., PROLONGED INFECTION OF MOUSE-BRAIN NEURONS WITH MURINE CYTOMEGALOVIRUS AFTER PRENATAL AND PERINATAL INFECTION, Archives of virology, 140(10), 1995, pp. 1725-1736
The susceptibility of mice at different developmental stages to a rela
tively low titer of cell culture-passaged murine cytomegalovirus (MCMV
) infection was compared in terms of the urinary excretion of MCMV exa
mined by plaque assay and in terms of the distribution of viral infect
ion, determined by immunohistochemistry, using antibodies specific to
the early nuclear antigen of MCMV. Viral infection on day 8.5 of gesta
tion (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. Embryona
l and perinatal mice were more susceptible to MCMV in terms of urinary
excretion of the virus and the presence of viral antigen-positive cel
ls in the brain, lungs, and kidneys. In the embryonal and perinatal in
fection, the viral antigen-positive cells in the neurons of the cerebr
al cortex and hippocampus were retained late after birth, even though
the positive cells in the lungs and kidneys had disappeared. In the mi
ce infected on E8.5, small clusters of viral antigen-positive cells we
re detected only in the cortex and hippocampus late after birth, witho
ut the urinary excretion of virus. These results suggest that when mic
e are infected with MCMV at the embryonal and perinatal stages, elimin
ation of the infected neurons is delayed compared with that of the oth
er cells in the lungs and kidneys. These findings provide a model for
the analysis of pathogenesis of the subclinical congenital CMV infecti
on that manifested clinically late after birth in humans as brain diso
rders.