Pathological observations on experimental cytomegalovirus infections in pregnancy

Lansdown, A. B. G.; Brown, Jacqueline D.

doi:10.1002/path.1711250102

Cited by 10 publications

(2 citation statements)

References 19 publications

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“…The functional diversity of these particles in relation to cell killing in vitro has not been fulIy explored nor has the significance of cell killing in vivo been considered in relation to the pathogenesis of CMV infections. There have been reports of splenic necrosis and depletion of thymus derived lymphoeytes in certain strains of mice infected with murine CMV (13,14). While in general these pathological manifestations did appear to correlate with virus replication in the spleen, a substantial drop in the number of nucleated spleen cells two to three days after inoculation, well before virus replication had reached its peak, could be interpreted as lymphoid cell killing without complete virus replication.…”

Section: Diseussionmentioning

confidence: 89%

Lymphoid cell killing by human cytomegalovirus

Riepenhoff-Talty

Flanagan

1982

Archives of Virology

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The interaction of human cytomegalovirus (CMV) with two replicating lymphoid cell lines, Ra-1 and MOLT-4F was studied. It was determined that while the cells exhibited viral receptors, the production of viral antigen and fully infectious virus could not be documented. Instead, cell death proportionate to the quantity of virus inoculated was seen. Neutralization of cell killing was effected with CMV-specific antiserum. In addition it was ascertained that cell death appeared to require a viral genomic function. This conclusion was based on the observation that UV irradiation of virus stocks reduced the cell killing capacity of the preparation. Infectivity of virus preparations was more sensitive to UV than the cell killing property. When compared on the basis of infectivity for fibroblasts and lymphoid cell killing capacity, pools of CMV with high infectivity had relatively less cell-killing capacity than low titered preparations.

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Section: Diseussionmentioning

confidence: 89%

Lymphoid cell killing by human cytomegalovirus

Riepenhoff-Talty

Flanagan

1982

Archives of Virology

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“…Animal models for congenital CMV infection have been reported using guinea pig CMV (GPCMV),i3' 4 murine CMV (MCMV) [15][16][17] and simian CMV.I8 -use transplacental transmission of GPCMV was demonstrated, extensive investigations have been reported as the model of congenital CMV i n f e c t i~n .~~-~' Guinea pigs possess a placenta with a single trophoblast layer simitar in structure to human placenta.z3…”

Section: ~X P E~i M~n T A~ Morels Of Congenital CMV Infectionmentioning

confidence: 99%

Developmental disorders of the mouse brain induced by murine cytomegalovirus: Animal models for congenital cytomegalovirus infection

Tsutsui

1995

Pathology International

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Developmental disorders induced by congenital cytomegalovirus (CMV) infection mainly involve the central nervous system. The type and degree of the brain disorders seems to depend on infection time during gestation, virulence, route of infection and viral susceptible cells in each embryonal stage. Since transplacental transmission has been reported not to occur with murine CMV (MCMV), we developed mouse models for congenital CMV infection by surgical injection of MCMV into the mouse conceptus or embryo at different gestational stages. For the early stage, the mouse embryos were not infected with MCMV even after injecting the virus into the blastocysts, which were developed in the pseudo-pregnant mothers or cultured in vitro. Isolated whole mouse embryos of day 7.5 of gestation (E7.5), adsorbed with a high titer of MCMV and cultured for 3 days, were susceptible to MCMV infection. Therefore, the mouse embryo acquires the susceptibility around this period. Microphthalmia and cerebral atrophy were induced in mouse embryos after injection of MCMV into the conceptus on E8.5. Viral antigen-positive cells were widely distributed in the mesenchyme around the oral and nasal cavities and in the mesenchyme around the brain, especially the endothelial cells of vessels and the perivascular mesodermal cells, then infection extends to the eyes, brain or choroid plexus. This finding suggests that mesenchymal infection may be the critical step in disrupting organogenesis, resulting in brain disorders. For the late stage, mouse embryos were infected with MCMV by injecting the virus into the cerebral ventricles on E15.5. Brains of the offspring showed massive necrosis with gliomesodermal proliferation in the cerebral cortex. Viral antigen-positive cells were observed in laminar array in the lesion-free cortex and the hippocampus, suggesting that the infected cells migrate in association with the lamina formation. Immunohistochemical double-staining showed that brain cells susceptible to MCMV infection may be mainly neuronal and endothelial cells, resulting in cerebral atrophy with reduction of neuronal cells and cystic lesions, presumably due to ischemic vascular changes.

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The effects of maternal murine cytomegalovirus infection on the mouse conceptus at different gestational stages

Huang

Chernoff

Kavlock

et al. 1986

Teratog Carcinog Mutagen

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The effects of murine cytomegalovirus (MCMV) on the prenatal development of the CD-1 mouse were investigated. Two sets of experiments were performed. In the first, mice were inoculated with different doses of MCMV on gestational day 7, and in the second, pregnant animals were inoculated with a subacute injection dose at different gestational stages. The effects of maternal infection on pregnancy in terms of maternal sickness, embryo lethality, date of parturition, litter size, postnatal death, and pups' body weight on d 1 and d 3 postpartum were investigated. High-dose MCMV infection on d 7 of pregnancy resulted in a significant increase in early embryo resorption and also in a reduction of the neonatal body weight of surviving pups. Two gestational stages were identified as being especially susceptible to MCMV infection. Most embryonic death as indicated by resorption rates was found after treatment on d 9, whereas perinatal death was most frequent when treatment was done on d 13 of gestation. Still births and neonatal death within 24 h of birth were found commonly in this latter group, which also showed the most pronounced growth retardation. The phenomenon of delay in time of parturition was noted and found to be most significant in groups of animals that were inoculated on d 3 or d 13. This investigation suggests that the effects of MCMV on the CD-1 mouse vary greatly with the age of the embryo and the course of the infection.

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Pathological observations on experimental cytomegalovirus infections in pregnancy

Cited by 10 publications

References 19 publications

Lymphoid cell killing by human cytomegalovirus

Lymphoid cell killing by human cytomegalovirus

Developmental disorders of the mouse brain induced by murine cytomegalovirus: Animal models for congenital cytomegalovirus infection

The effects of maternal murine cytomegalovirus infection on the mouse conceptus at different gestational stages

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