Regulation of transplacental virus infection by developmental and immunological factors: studies with lactate dehydrogenase-elevating virus

Haven, Thomas R.; Rowland, Raymond R. R.; Plagemann, Peter G.W.; Wong, Grace; Bradley, Sarahann; Cafruny, William A.

doi:10.1016/0168-1702(96)01283-x

Cited by 13 publications

(8 citation statements)

References 19 publications

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“…The virus spread occurred despite expression of at least one isotype of IFN-in all the maternal tissues examined and in the absence of detectable vascular endothelial cell infection, suggesting that the virus may initially be transported intracellularly from the site of infection to susceptible target tissues. 2,14 Previous studies have also pointed to a tissue establishment phase, with cyclic appearance and disappearance of viremia. 16 In one study, 19 virus was detected only in the placentomes of ewes (pregnant for 34-45 days) at 4 days postinoculation (d.p.i.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, either the placenta acts as a barrier to fetal infection or the fetus may be ''resistant'' to the infection. 14 The placental barrier may be due to efficient innate immunologic surveillance mechanisms in the maternal tissues, 5,10 and fetal resistance may be exerted by antiviral agents secreted by the conceptus 21,22 or the lack of virus permissive cells at any one particular stage of fetal development. 14 However, once fetal infection is established the range of outcomes is vast, with abortion, stillbirth, congenital malformations, and growth retardation described for a variety of viruses.…”

Section: Discussionmentioning

confidence: 99%

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Rapid Transplacental Infection with Bovine Pestivirus Following Intranasal Inoculation of Ewes in Early Pregnancy

et al. 2001

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Abstract. Despite the importance of congenital viral infections in both veterinary and human medicine, only limited experimental work has been carried out to elucidate the mechanisms involved in transplacental virus infections. To further an understanding of fetal infection with pestiviruses, the distribution of bovine pestivirus in the uterine and fetal tissues of ewes in early pregnancy, following a natural route of infection, was investigated. On the 18th day of pregnancy, nine ewes were inoculated by the intranasal route with 1 ϫ 10 5 50% tissue culture infective doses of an Australian isolate of noncytopathic bovine pestivirus (bovine viral diarrhea virus genotype 1). All ewes were ovariohysterectomized at approximately 100 hours postinfection. Samples from the reproductive tract and conceptus were examined histologically and tested for bovine pestivirus by nested reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry and for interferon-tau mRNA expression by nonnested RT-PCR. Although no histopathologic changes were observed in the maternal or fetal tissues, virus was detected in the reproductive tract of all nine ewes and in all of the conceptuses examined. At the time of surgery, only two of the nine ewes were demonstrably viremic. This study demonstrates that bovine pestivirus can spread from a natural site of infection to the ovine fetus within 4 days in the absence of maternal immunity and despite the presence of interferon expression in the reproductive tract.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Rapid Transplacental Infection with Bovine Pestivirus Following Intranasal Inoculation of Ewes in Early Pregnancy

et al. 2001

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“…Murine models have also shown that fetal outcomes are influenced by maternal immune status and timing of the infection (41,42). For example, transplacental transmission of lactate dehydrogenase-elevating virus is highly efficient unless the mother is immune, or if the initial infection occurs before 13 days of gestation in nonimmune mice after which, the increased presence of infected macrophages at the maternal-fetal interface contribute to fetal transmission (42). Although pregnancy outcomes were not the primary focus of the study, our model could serve to investigate other immunologic mechanisms during the perinatal period.…”

Section: Discussionmentioning

confidence: 99%

Normal Establishment of Virus-Specific Memory CD8 T Cell Pool following Primary Infection during Pregnancy

Constantin¹,

Masopust

Gourley

et al. 2007

The Journal of Immunology

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Suppression of cell-mediated immunity has been proposed as a mechanism that promotes maternal tolerance of the fetus but also contributes to increased occurrence and severity of certain infections during pregnancy. Despite decades of research examining the effect of pregnancy on Ag-specific T cell responses, many questions remain. In particular, quantitative examination of memory CD8 T cell generation following infection during pregnancy remains largely unknown. To examine this issue, we evaluated the generation of protective immunity following infection during pregnancy with a nonpersistent strain of lymphocytic choriomeningitis virus (LCMV) in mice. The CD8 T cell response to LCMV occurred normally in pregnant mice compared with the nonpregnant cohort with rapid viral clearance in all tissues tested except for the placenta. Despite significant infiltration of CD8 T cells to the maternal-fetal interface, virus persisted in the placenta until delivery. Live pups were not infected and generated normal primary immune responses when challenged as adults. Memory CD8 T cell development in mice that were pregnant during primary infection was normal with regards to the proliferative capacity, number of Ag-specific cells, cytokine production upon re-stimulation, and the ability to protect from re-infection. These data suggest that virus-specific adaptive memory is normally generated in mice during pregnancy.

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“…Fetuses were protected from macrophage penetration, most likely due to their protective membranes (Rugh, 1969). A barrier to fetal entry is also consistent with immunological protection of fetuses observed when the mother is both LDV-infected and immune (Broen et al, 1992;Haven et al, 1996). Such protection would not be expected if LDV-infected macrophages were able to enter the fetus.…”

Section: Discussionmentioning

confidence: 50%

Trojan Horse macrophages: studies with the murine lactate dehydrogenase-elevating virus and implications for sexually transmitted virus infection

Cafruny

Bradley²

1996

Journal of General Virology

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Regulation of transplacental virus infection by developmental and immunological factors: studies with lactate dehydrogenase-elevating virus

Cited by 13 publications

References 19 publications

Rapid Transplacental Infection with Bovine Pestivirus Following Intranasal Inoculation of Ewes in Early Pregnancy

Rapid Transplacental Infection with Bovine Pestivirus Following Intranasal Inoculation of Ewes in Early Pregnancy

Normal Establishment of Virus-Specific Memory CD8 T Cell Pool following Primary Infection during Pregnancy

Trojan Horse macrophages: studies with the murine lactate dehydrogenase-elevating virus and implications for sexually transmitted virus infection

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