Is fetal gender a risk factor for severe congenital cytomegalovirus infection?
Identifieur interne : 000208 ( France/Analysis ); précédent : 000207; suivant : 000209Is fetal gender a risk factor for severe congenital cytomegalovirus infection?
Auteurs : Olivier Picone [France] ; Jean-Marc Costa [France] ; Anne Dejean [France] ; Yves Ville [France]Source :
- Prenatal Diagnosis [ 0197-3851 ] ; 2005-01.
English descriptors
- Teeft :
- Abnormal brain development, Asymptomatic, Boppana, Brain abnormalities, Brain anomalies, Brain development, Cerebral microcephaly, Cerebral ventriculomegaly, Clin microbiol, Congenital, Congenital cytomegalovirus infection, Congenital infection, Cytomegalic inclusion disease, Cytomegalovirus, Cytomegalovirus infection, Diagn, Fetal, Fetal cytomegalovirus infection, Fetal gender, Fetal infection, Fetus, Gender, Gynecol, Host genetics, Infection, Intrauterine cytomegalovirus infection, John wiley sons, Main cause, Ndings, Neurological impairment, Obstet, Obstet gynecol, Pediatr, Pediatric cohorts, Precursor cells, Prenat, Prenat diagn, Prenatal, Prenatal diagnosis, Primary infection, Psychomotor development, Risk factor, Subependymal cysts, Table ratio, Ultrasound, Ultrasound obstet gynecol, Vertical transmission rate, Viral, Viral infection, Viral load.
Abstract
Cytomegalovirus is the main cause of congenital viral infection and amniotic fluid viral load appears to be the single nonclinical prognostic factor. However, as in other infectious diseases, host genetics may influence the severity of the disease. To test this hypothesis, we looked retrospectively at the fetal gender in cases of severe congenital cytomegalovirus infection in our database. We also analyzed the international English literature covering this subject between 1985 and 2003. The proportion of females with brain abnormalities was statistically different from that of males (62/258: 24% vs 30/251: 12%, p = 0.004). The risk of abnormal brain development in infected fetuses was twice as high in females than in males (Chi2 = 8.7; OR = 2, IC [1.26–3.21]). In our cases, amniotic fluid CMV DNA load was not significantly higher in males than in females (p = 0.06) and was also similar in severely and non‐severely infected fetuses (p = 0.09). Copyright © 2005 John Wiley & Sons, Ltd.
Url:
DOI: 10.1002/pd.944
Affiliations:
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Américain de Paris, Neuilly‐sur‐Seine</wicri:regionArea><wicri:noRegion>Neuilly‐sur‐Seine</wicri:noRegion><wicri:noRegion>Neuilly‐sur‐Seine</wicri:noRegion></affiliation></author><author><name sortKey="Dejean, Anne" sort="Dejean, Anne" uniqKey="Dejean A" first="Anne" last="Dejean">Anne Dejean</name><affiliation wicri:level="1"><country xml:lang="fr">France</country><wicri:regionArea>Service de Gynécologie Obstétrique, CHI Poissy‐St‐Germain</wicri:regionArea><wicri:noRegion>CHI Poissy‐St‐Germain</wicri:noRegion><wicri:noRegion>CHI Poissy‐St‐Germain</wicri:noRegion></affiliation></author><author><name sortKey="Ville, Yves" sort="Ville, Yves" uniqKey="Ville Y" first="Yves" last="Ville">Yves Ville</name><affiliation wicri:level="1"><country xml:lang="fr">France</country><wicri:regionArea>Service de Gynécologie Obstétrique, CHI Poissy‐St‐Germain</wicri:regionArea><wicri:noRegion>CHI Poissy‐St‐Germain</wicri:noRegion><wicri:noRegion>CHI Poissy‐St‐Germain</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Prenatal Diagnosis</title><title level="j" type="alt">PRENATAL DIAGNOSIS</title><idno type="ISSN">0197-3851</idno><idno type="eISSN">1097-0223</idno><imprint><biblScope unit="vol">25</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="34">34</biblScope><biblScope unit="page" to="38">38</biblScope><biblScope unit="page-count">5</biblScope><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2005-01">2005-01</date></imprint><idno type="ISSN">0197-3851</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0197-3851</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Abnormal brain development</term><term>Asymptomatic</term><term>Boppana</term><term>Brain abnormalities</term><term>Brain anomalies</term><term>Brain development</term><term>Cerebral microcephaly</term><term>Cerebral ventriculomegaly</term><term>Clin microbiol</term><term>Congenital</term><term>Congenital cytomegalovirus infection</term><term>Congenital infection</term><term>Cytomegalic inclusion disease</term><term>Cytomegalovirus</term><term>Cytomegalovirus infection</term><term>Diagn</term><term>Fetal</term><term>Fetal cytomegalovirus infection</term><term>Fetal gender</term><term>Fetal infection</term><term>Fetus</term><term>Gender</term><term>Gynecol</term><term>Host genetics</term><term>Infection</term><term>Intrauterine cytomegalovirus infection</term><term>John wiley sons</term><term>Main cause</term><term>Ndings</term><term>Neurological impairment</term><term>Obstet</term><term>Obstet gynecol</term><term>Pediatr</term><term>Pediatric cohorts</term><term>Precursor cells</term><term>Prenat</term><term>Prenat diagn</term><term>Prenatal</term><term>Prenatal diagnosis</term><term>Primary infection</term><term>Psychomotor development</term><term>Risk factor</term><term>Subependymal cysts</term><term>Table ratio</term><term>Ultrasound</term><term>Ultrasound obstet gynecol</term><term>Vertical transmission rate</term><term>Viral</term><term>Viral infection</term><term>Viral load</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cytomegalovirus is the main cause of congenital viral infection and amniotic fluid viral load appears to be the single nonclinical prognostic factor. However, as in other infectious diseases, host genetics may influence the severity of the disease. To test this hypothesis, we looked retrospectively at the fetal gender in cases of severe congenital cytomegalovirus infection in our database. We also analyzed the international English literature covering this subject between 1985 and 2003. The proportion of females with brain abnormalities was statistically different from that of males (62/258: 24% vs 30/251: 12%, p = 0.004). The risk of abnormal brain development in infected fetuses was twice as high in females than in males (Chi2 = 8.7; OR = 2, IC [1.26–3.21]). In our cases, amniotic fluid CMV DNA load was not significantly higher in males than in females (p = 0.06) and was also similar in severely and non‐severely infected fetuses (p = 0.09). 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