The Placental Response to Guinea Pig Cytomegalovirus Depends Upon the Timing of Maternal Infection
| Autor: | Mark R. Schleiss, Juan E. Abrahante, Davis M. Seelig, Zachary W. Berkebile, Dira S. Putri, Craig J. Bierle |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Human cytomegalovirus placenta Guinea Pigs Immunology Congenital cytomegalovirus infection Cytomegalovirus Biology Andrology 03 medical and health sciences fetal membranes 0302 clinical medicine Pregnancy Placenta medicine Animals Immunology and Allergy Pregnancy Complications Infectious Original Research Fetus 030219 obstetrics & reproductive medicine Transplacental RC581-607 Viral Load medicine.disease congenital infection 030104 developmental biology medicine.anatomical_structure inflammation Cytomegalovirus Infections Gestation Female Immunologic diseases. Allergy Viral load guinea pig |
| Zdroj: | Frontiers in Immunology Frontiers in Immunology, Vol 12 (2021) |
| ISSN: | 1664-3224 |
| Popis: | Human cytomegalovirus (HCMV) infects the placenta, and these placental infections can cause fetal injury and/or demise. The timing of maternal HCMV infection during pregnancy is a determinant of fetal outcomes, but how development affects the placenta’s susceptibility to infection, the likelihood of placental injury post-infection, and the frequency of transplacental HCMV transmission remains unclear. In this study, guinea pig cytomegalovirus (GPCMV) was used to model primary maternal infection and compare the effects of infection at two different times on the placenta. When guinea pigs were infected with GPCMV at either 21- or 35-days gestation (dGA), maternal and placental viral loads, as determined by droplet digital PCR, were not significantly affected by the timing of maternal infection. However, when the transcriptomes of gestational age-matched GPCMV-infected and control placentas were compared, significant infection-associated changes in gene expression were only observed after maternal infection at 35 dGA. Notably, transcripts associated with immune activation (e.g. Cxcl10, Ido1, Tgtp1, and Tlr8) were upregulated in the infected placenta. A GPCMV-specific in situ hybridization assay detected rare infected cells in the main placenta after maternal infection at either time, and maternal infection at 35 dGA also caused large areas of GPCMV-infected cells in the junctional zone. As GPCMV infection after mid-gestation is known to cause high rates of stillbirth and/or fetal growth restriction, our results suggest that the placenta becomes sensitized to infection-associated injury late in gestation, conferring an increased risk of adverse pregnancy outcomes after cytomegalovirus infection. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|