Abstract
Background. Human cytomegalovirus (HCMV) is the major viral etiology of congenital infection and birth defects. Fetal transmission is high (30%-40%) in primary maternal infection, and symptomatic babies have permanent neurological, hearing, and vision defects. Recurrent infection is infrequently transmitted (2%) and largely asymptomatic. Congenital infection is also associated with intrauterine growth restriction (IUGR). Methods. To investigate possible underlyingHCMVinfection in cases of idiopathic IUGR,we studiedmaternal and cord sera and placentas from 19 pregnancies. Anti-HCMVantibodies, hypoxia-related factors, and cmvIL-10 weremeasuredinsera. Placental biopsyspecimenswere examined for viralDNA, expressionof infectedcell proteins, and pathology. Results. Among 7 IUGR cases, we identified 2 primary and 3 recurrent HCMV infections. Virus replicated in glandular epitheliumand lymphatic endotheliumin the decidua, cytotrophoblasts, and smoothmuscle cells in blood vessels of floating villi and the chorion. Large fibrinoids with avascular villi, edema, and inflammation were significantly increased. Detectionofviralproteinsintheamnioticepitheliumindicatedtransmissionin2cases ofIUGRwithprimaryinfectionand 3 asymptomatic recurrent infections. Conclusions. CongenitalHCMVinfectionimpairs placentaldevelopmentand functions and shouldbe consideredas an underlying cause of IUGR, regardless of virus transmission to the fetus.
| Original language | English |
|---|---|
| Pages (from-to) | 1573-1584 |
| Number of pages | 12 |
| Journal | Journal of Infectious Diseases |
| Volume | 209 |
| Issue number | 10 |
| DOIs | |
| Publication status | Published - May 15 2014 |
| Externally published | Yes |
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Keywords
- amnion
- blood vessels
- chorion
- congenital
- fetus
- HCMV
- IUGR
- placenta
- pregnancy
- villi
ASJC Scopus subject areas
- Immunology and Allergy
- Infectious Diseases
Cite this
Intrauterine growth restriction caused by underlying congenital cytomegalovirus infection. / Pereira, Lenore; Petitt, Matthew; Fong, Alex; Tsuge, Mitsuru; Tabata, Takako; Fang-Hoonver, June; Maidji, Ekaterina; Zydek, Martin; Zhou, Yan; Inoue, Naoki; Loghavi, Sanam; Pepkowitz, Samuel; Kauvar, Lawrence M.; Ogunyemi, Dotun.
In: Journal of Infectious Diseases, Vol. 209, No. 10, 15.05.2014, p. 1573-1584.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Intrauterine growth restriction caused by underlying congenital cytomegalovirus infection
AU - Pereira, Lenore
AU - Petitt, Matthew
AU - Fong, Alex
AU - Tsuge, Mitsuru
AU - Tabata, Takako
AU - Fang-Hoonver, June
AU - Maidji, Ekaterina
AU - Zydek, Martin
AU - Zhou, Yan
AU - Inoue, Naoki
AU - Loghavi, Sanam
AU - Pepkowitz, Samuel
AU - Kauvar, Lawrence M.
AU - Ogunyemi, Dotun
PY - 2014/5/15
Y1 - 2014/5/15
N2 - Background. Human cytomegalovirus (HCMV) is the major viral etiology of congenital infection and birth defects. Fetal transmission is high (30%-40%) in primary maternal infection, and symptomatic babies have permanent neurological, hearing, and vision defects. Recurrent infection is infrequently transmitted (2%) and largely asymptomatic. Congenital infection is also associated with intrauterine growth restriction (IUGR). Methods. To investigate possible underlyingHCMVinfection in cases of idiopathic IUGR,we studiedmaternal and cord sera and placentas from 19 pregnancies. Anti-HCMVantibodies, hypoxia-related factors, and cmvIL-10 weremeasuredinsera. Placental biopsyspecimenswere examined for viralDNA, expressionof infectedcell proteins, and pathology. Results. Among 7 IUGR cases, we identified 2 primary and 3 recurrent HCMV infections. Virus replicated in glandular epitheliumand lymphatic endotheliumin the decidua, cytotrophoblasts, and smoothmuscle cells in blood vessels of floating villi and the chorion. Large fibrinoids with avascular villi, edema, and inflammation were significantly increased. Detectionofviralproteinsintheamnioticepitheliumindicatedtransmissionin2cases ofIUGRwithprimaryinfectionand 3 asymptomatic recurrent infections. Conclusions. CongenitalHCMVinfectionimpairs placentaldevelopmentand functions and shouldbe consideredas an underlying cause of IUGR, regardless of virus transmission to the fetus.
AB - Background. Human cytomegalovirus (HCMV) is the major viral etiology of congenital infection and birth defects. Fetal transmission is high (30%-40%) in primary maternal infection, and symptomatic babies have permanent neurological, hearing, and vision defects. Recurrent infection is infrequently transmitted (2%) and largely asymptomatic. Congenital infection is also associated with intrauterine growth restriction (IUGR). Methods. To investigate possible underlyingHCMVinfection in cases of idiopathic IUGR,we studiedmaternal and cord sera and placentas from 19 pregnancies. Anti-HCMVantibodies, hypoxia-related factors, and cmvIL-10 weremeasuredinsera. Placental biopsyspecimenswere examined for viralDNA, expressionof infectedcell proteins, and pathology. Results. Among 7 IUGR cases, we identified 2 primary and 3 recurrent HCMV infections. Virus replicated in glandular epitheliumand lymphatic endotheliumin the decidua, cytotrophoblasts, and smoothmuscle cells in blood vessels of floating villi and the chorion. Large fibrinoids with avascular villi, edema, and inflammation were significantly increased. Detectionofviralproteinsintheamnioticepitheliumindicatedtransmissionin2cases ofIUGRwithprimaryinfectionand 3 asymptomatic recurrent infections. Conclusions. CongenitalHCMVinfectionimpairs placentaldevelopmentand functions and shouldbe consideredas an underlying cause of IUGR, regardless of virus transmission to the fetus.
KW - amnion
KW - blood vessels
KW - chorion
KW - congenital
KW - fetus
KW - HCMV
KW - IUGR
KW - placenta
KW - pregnancy
KW - villi
UR - http://www.scopus.com/inward/record.url?scp=84897911317&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84897911317&partnerID=8YFLogxK
U2 - 10.1093/infdis/jiu019
DO - 10.1093/infdis/jiu019
M3 - Article
VL - 209
SP - 1573
EP - 1584
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
SN - 0022-1899
IS - 10
ER -