| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Regular Article |
a Center for Research on Reproduction and Women's Health, Department of Obstetrics and Gynecology, University of Pennsylvania, Philadelphia, Pennsylvania 19104
b Department of Obstetrics and Gynecology, University of British Columbia, Vancouver, British Columbia, Canada V5Z4H4
ABSTRACT
The molecular mechanisms and pathologic significance of placental viral infections are poorly understood. We investigated factors that regulate placental infection by adenovirus, which is the most common viral pathogen identified in fetal samples from abnormal pregnancies (i.e., fetal growth restriction, oligohydramnios, and nonimmune fetal hydrops). We also determined the pathologic significance of placental adenovirus infection. Northern hybridization, flow cytometry, and immunostaining revealed that placental expression of the coxsackievirus and adenovirus receptor (CAR) varied with gestational age and trophoblast phenotype. The CAR was continuously expressed in invasive or extravillous trophoblast cells but not in villous trophoblast cells. We postulate that the villous syncytiotrophoblast, which does not express CAR and is resistant to adenovirus infection, limits the transplacental transmission of viral pathogens, including adenovirus. Conversely, extravillous trophoblast cells underwent apoptosis when infected by adenovirus in the presence of decidual lymphocytes (which simulated the maternal immune response to viral infection). Thus, adenovirus infection and/or the maternal immune response to adenovirus infection induced the death of placental cell types that expressed CAR. Consequently, we speculate that adenovirus infection of extra-villous trophoblast cells may negatively impact the process of placental invasion and predispose the mother and fetus to adverse reproductive outcomes that result from placental dysfunction.
1 S.P. was supported by a Women's Reproductive Health Research Award provided by the NICHD and by the Thomas B. McCabe and Jeannette E. Laws McCabe Fund at the University of Pennsylvania. J.F.S. was supported by the Bill and Melinda Gates Foundation. G.S.K. was supported by HD06274, HD22732, and HD33052.
2 Correspondence: Samuel Parry, 1352 Biomedical Research Building II/III, 421 Curie Boulevard, Philadelphia, PA 19104-6142. FAX: 215 573 5408; parry{at}mail.med.upenn.edu
This article has been cited by other articles:
|
|
 |
|
  F. Arechavaleta-Velasco, Y. Ma, J. Zhang, C. M. McGrath, and S. Parry Adeno-Associated Virus-2 (AAV-2) Causes Trophoblast Dysfunction, and Placental AAV-2 Infection Is Associated with Preeclampsia Am. J. Pathol., June 1, 2006; 168(6): 1951 - 1959. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. A. Dorner, F. Wegmann, S. Butz, K. Wolburg-Buchholz, H. Wolburg, A. Mack, I. Nasdala, B. August, J. Westermann, F. G. Rathjen, et al. Coxsackievirus-adenovirus receptor (CAR) is essential for early embryonic cardiac development J. Cell Sci., August 1, 2005; 118(15): 3509 - 3521. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Terauchi, H. Koi, C. Hayano, N. Toyama-Sorimachi, H. Karasuyama, Y. Yamanashi, T. Aso, and M. Shirakata Placental Extravillous Cytotrophoblasts Persistently Express Class I Major Histocompatibility Complex Molecules after Human Cytomegalovirus Infection J. Virol., August 1, 2003; 77(15): 8187 - 8195. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. KOI, J. ZHANG, and S. PARRY The Mechanisms of Placental Viral Infection Ann. N.Y. Acad. Sci., September 1, 2001; 943(1): 148 - 156. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
