New estimates of the prevalence of neurological and sensory sequelae and mortality associated with congenital cytomegalovirus infection

Dollard, Sheila C.; Grosse, Scott D.; Ross, Danielle S.

doi:10.1002/rmv.544

Cited by 1,025 publications

(1,064 citation statements)

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“…2,3 Thus, at least 1 in every 500 newborns will exhibit major CMV-induced congenital pathology, making CMV one of the most common causes of major birth defects in humans (http://www.cdc.gov/cmv). 2,3 It has been established that about 36% of children with CMV-induced birth defects and 5% of CMV-infected asymptomatic infants also exhibit enamel hypoplasia and hypocalcification of the teeth. 4-7 In many cases, the enamel is absent and affected teeth tend to wear down rapidly or to fracture.…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus inhibition of embryonic mouse tooth development: A model of the human amelogenesis imperfecta phenocopy

Jaskoll

Abichaker

Jangaard

et al. 2008

Archives of Oral Biology

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Objective-Cytomegalovirus (CMV) is one of the most common causes of major birth defects in humans. Of the approximately 8400 children born each year in the U.S. with CMV-induced birth defects, more than 1/3 of these children exhibit hypoplasia and hypocalcification of tooth enamel. Our objective was to initiate the investigation of the pathogenesis of CMV-induced tooth defects. Design-MouseCap stage mandibular first molars were infected with mouse CMV (mCMV) in vitro in a chemically-defined organ culture system and analysed utilising histological and immunolocalisation methodologies. The antiviral, acyclovir, was used to inhibit mCMV replication and comparisons made between mCMV-infected and acyclovir-treated, mCMV-infected teeth.Results-Active infection of Cap stage molars for up to 15 days in vitro results in smaller, developmentally-delayed and dysmorphic molars characterised by shallow, broad and misshapen cusps, infected and affected dental papilla mesenchyme, poorly differentiated odontoblasts and ameloblasts, and no dentin matrix. Initial protein localisation studies suggest that the pathogenesis is mediated through NF-κB signaling and that there appears to be an unusual interaction between abnormal mesenchymal cells and surrounding matrix. Rescue with acyclovir indicates that mCMV replication is necessary to initiate and sustain progressive tooth dysmorphogenesis.Conclusions-Our results indicate that mCMV-induced changes in signaling pathways severely delays, but does not completely interrupt, tooth morphogenesis. Importantly, our results demonstrate that this well-defined embryonic mouse organ culture system can be utilised to delineate the molecular mechanism underlying the CMV-induced tooth defects that characterise the amelogenesis imperfecta phenocopy seen in many CMV-infected children.

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Section: Introductionmentioning

confidence: 99%

Cytomegalovirus inhibition of embryonic mouse tooth development: A model of the human amelogenesis imperfecta phenocopy

Jaskoll

Abichaker

Jangaard

et al. 2008

Archives of Oral Biology

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“…1,2 Approximately 20% of these infected newborns are symptomatic at birth or will have sequelae such as sensorineural hearing loss, cognitive defects, and motor defects. 3 Primary CMV infection that develops in a woman during pregnancy confers the highest risk of congenital infection and disease. 4 Identification of pregnant women with primary CMV infection is feasible by means of detection of virus-specific IgM and low IgG avidity.…”

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confidence: 99%

A Randomized Trial of Hyperimmune Globulin to Prevent Congenital Cytomegalovirus

Revello¹,

et al. 2014

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Congenital infection with human cytomegalovirus (CMV) is a major cause of morbidity and mortality. In an uncontrolled study published in 2005, administration of CMV-specific hyperimmune globulin to pregnant women with primary CMV infection\ud significantly reduced the rate of intrauterine transmission, from 40% to 16%. Methods: We evaluated the efficacy of hyperimmune globulin in a phase 2, randomized, placebo-controlled, double-blind study. A total of 124 pregnant women with primary\ud CMV infection at 5 to 26 weeks of gestation were randomly assigned within 6 weeks after the presumed onset of infection to receive hyperimmune globulin or placebo every 4 weeks until 36 weeks of gestation or until detection of CMV in amniotic fluid. The primary end point was congenital infection diagnosed at birth\ud or by means of amniocentesis. Results: A total of 123 women could be evaluated in the efficacy analysis (1 woman in the\ud placebo group withdrew). The rate of congenital infection was 30% (18 fetuses or infants of 61 women) in the hyperimmune globulin group and 44% (27 fetuses or infants of 62 women) in the placebo group (a difference of 14 percentage points; 95% confidence interval, −3 to 31; P = 0.13). There was no significant difference\ud between the two groups or, within each group, between the women who transmitted the virus and those who did not, with respect to levels of virus-specific antibodies, T-cell–mediated immune response, or viral DNA in the blood. The clinical\ud outcome of congenital infection at birth was similar in the two groups. The number of obstetrical adverse events was higher in the hyperimmune globulin group than in the placebo group (13% vs. 2%). Conclusions: In this study involving 123 women who could be evaluated, treatment with hyperimmune globulin did not significantly modify the course of primary CMV infection during pregnancy. (Funded by Agenzia Italiana del Farmaco; CHIP ClinicalTrials.gov number, NCT00881517; EudraCT no. 2008-006560-11.

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“…In neonates, the symptoms include intrauterine growth retardation, microcephaly with intracranial calcification, hepatosplenomegaly, jaundice, chorioretinitis, thrombocytopenic purpura, and anemia [9]. The major childhood disabilities like loss of vision, hearing, and cognitive impairment are also due to CMV infection [10].…”

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confidence: 99%

Seroprevalence and Influence of Torch Infections in High Risk Pregnant Women: A Large Study from South India

Prasoona

Buragadda

Sunitha

et al. 2014

J Obstet Gynecol India

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Background The increased complications to the mother and fetus during or after pregnancy and birth are often caused by a wide array of pathogenic organisms mostly belonging to the TORCH group [toxoplasmosis, rubella, cytomegalovirus (CMV), and herpes simplex virus (HSV)]. These agents cause asymptomatic or mild infection in the mother while serious consequences in fetus. The present study was aimed to find significant etiological pathogens in the causation of high risk pregnancy (HRP) in South Indian population. Material and Methods A total of 1, 158 HRP women (2010158 HRP women ( -2013 from Modern Government Maternity Hospital, Hyderabad were considered. Two milliliter of blood was obtained and the serum was analyzed for IgG and IgM antibodies against TORCH agents by ELISA. Results Twenty-five percent of the study group had fetal congenital malformation in the present pregnancy (Group 1; N = 291) while 75 % showed bad obstetric history (BOH) (Group 2; N = 867). Maternal age of B25 years, primi gravida, and consanguinity showed predisposing role for Group 1 while maternal age C30 years and C 3 gravida were contributing risk for Group 2. The seropositvity in 123HRP women for toxoplasma, rubella, CMV, and HSV was 28, 84, 92, and 61 %, respectively for IgG while it was 6, 3, 4, and 3 % for IgG ? IgM. Total seropositvity of toxoplasma, rubella, CMV, and HSV in Group 1 was 29, 97, 97, and 62 % while it was 36, 84, 97, and 65 % in Group 2, respectively. Conclusion Maternal age of B25 years, primi gravida, and consanguinity contributed to fetal congenital malformation in the present pregnancy while maternal age of C30 years and C 3 gravida towards BOH. Toxoplasma is protective while rubella and CMV are the infectious agents for HRP. Among the groups, toxoplasma and rubella conferred a predisposing risk towards Group 2 and Group 1, respectively. Sixty-one percent seropositvity of HSV in relation to bad obstetric outcome is the highest prevalence reported so far in India.

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New estimates of the prevalence of neurological and sensory sequelae and mortality associated with congenital cytomegalovirus infection

Cited by 1,025 publications

References 35 publications

Cytomegalovirus inhibition of embryonic mouse tooth development: A model of the human amelogenesis imperfecta phenocopy

Cytomegalovirus inhibition of embryonic mouse tooth development: A model of the human amelogenesis imperfecta phenocopy

A Randomized Trial of Hyperimmune Globulin to Prevent Congenital Cytomegalovirus

Seroprevalence and Influence of Torch Infections in High Risk Pregnant Women: A Large Study from South India

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