Journal
JOURNAL OF VIROLOGY
Volume 77, Issue 24, Pages 13301-13314Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.77.24.13301-13314.2003
Keywords
-
Categories
Funding
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P01HD030367] Funding Source: NIH RePORTER
- NATIONAL EYE INSTITUTE [R01EY013683] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R56AI046657, R01AI046657, R21AI053782] Funding Source: NIH RePORTER
- NEI NIH HHS [R01 EY013683, EY13683] Funding Source: Medline
- NIAID NIH HHS [R56 AI046657, R01 AI046657, AI53782, R21 AI053782, AI46657] Funding Source: Medline
- NICHD NIH HHS [HD30367, P01 HD030367] Funding Source: Medline
Ask authors/readers for more resources
Prenatal cytomegalovirus infection may cause pregnancy complications such as intrauterine growth restriction and birth defects. How virus from the mother traverses the placenta is unknown. PCR analysis of biopsy specimens of the maternal-fetal interface revealed that DNA sequences from cytomegalovirus were commonly found with those of herpes simplex viruses and pathogenic bacteria. Cytomegalovirus DNA and infected cell proteins were found more often in the decidua than in the placenta, suggesting that the uterus functions as a reservoir for infection. In women with low neutralizing titers, cytomegalovirus replicated in diverse decidual cells and placental trophoblasts and capillaries. In women with intermediate to high neutralizing titers, decidual infection was suppressed and the placenta was spared. Overall, cytomegalovirus virions and maternal immunoglobulin G were detected in syncytiotrophoblasts, villus core macrophages, and dendritic cells. These results suggest that the outcome of cytomegalovirus infection depends on the presence of other pathogens and coordinated immune responses to viral replication at the maternal-fetal interface.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available