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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seroconversion to cytomegalovirus occurs in 1-4% of pregnant women, most of whom are seropositive prior to pregnancy. In 0.2-2.5% of their newborn infants there is evidence of intrauterine infection; most are born without any clinical findings The typical clinical symptoms of symptomatic congenital CMV are observed in 10-20% of infected neonates. They include intrauterine growth restriction, microcephaly, hepatosplenomegaly, petechiae, jaundice, thrombocytopenia, anemia, chorioretinitis, hearing loss and/or other findings. Long-term neurodevelopmental sequelae include mental retardation, motor impairment, sensorineural hearing loss and/or visual impairment. These may occur even in infants who are free of symptoms at birth. Most infants born with severe neonatal symptoms of congenital CMV are born to mothers with primary infection during pregnancy. However, since about half of the infants infected with CMV in utero, including those with severe neonatal symptoms, are born to mothers with preconceptional immunity, we have to conclude that congenital CMV may be a significant problem even in children born to mothers with pre-pregnancy immunization. This may justify the use of invasive methods for the detection of possible fetal infection even in cases of non-primary CMV infection. This should also be a consideration when deciding upon population screening or immunization for CMV.
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PMID:Fetal effects of primary and non-primary cytomegalovirus infection in pregnancy: are we close to prevention? 1759 85

Cytomegalovirus (CMV) is the leading cause of congenital viral infection, with an incidence of 0.5-3% of live births worldwide. Clinical evidence has shown hearing and vision loss, mental retardation and sometimes death in affected newborns. Primary maternal CMV infection during gestation poses a 40% risk of intrauterine transmission in contrast to recurrent infection. European laboratories have made significant progress in the last decade in solving diagnostic problems linked to infection in pregnancy. With the advances in CMV serology, such as detection of anti-CMV IgM by enzyme immunoassays (EIA), confirmed by Western blot, together with seroconversion and anti-CMV IgG avidity evaluation in pregnant mothers, can help to identify recent infection. Preventative measures such as screening for CMV in the routine serological work-up of pregnant women have been introduced in countries such as Spain and Italy. The development of specific T cell-mediated immune responses in mothers, fetus and neonates is now emerging with regard to antigen-specific CD4 and CD8 T cells, differentiation status, proliferative and cytokine responses. A protective vaccine against CMV is a major public health priority and the study of vaccines in animal model systems has identified potential strategies for interrupting transmission and preventing disease in newborns. Congenital CMV infection has a variable outcome and therefore novel diagnostic methods are required to identify those at risk and therapeutic interventions are needed to improve the long-term prognosis of those infected. CMV was first isolated in 1957. We are now 50 years on, so procrastination is not an option.
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PMID:Translational mini-review series on infectious disease: congenital cytomegalovirus infection: 50 years on. 1763 29

Human Cytomegalovirus (CMV) is the main cause of mental retardation and sensorineural hearing loss related to congenital infections. Justification of systematic screening for fetal CMV infection is still controversial and is not recommended in most developed countries. This is mainly justified by the paucity of antenatal prognostic factors and the lack of established intrauterine treatment when fetal infection has been diagnosed. Our aim was to review the current state of the knowledge about the CMV congenital infection and to highlight recent advances in the diagnosis as well as in the identification of prognostic factors.
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PMID:[Cytomegalovirus (CMV) congenital infection]. 1833 44

Cytomegalovirus (CMV) is the most significant infectious cause of brain disorders in humans. Although the brain is the principal target organ for CMV infection in infants with congenital infection and in immunocompromised patients, little has been known about cellular events in pathogenesis of the brain disorders. Mouse models have been developed by the authors for studying the cell tropism, infectious dynamics of CMV infection and the effects of CMV infection on proliferation, regeneration and differentiation of neural cells. It has been shown, using brain slice cultures and neurospheres, that neural stem progenitor (NSP) cells are the most susceptible to CMV infection in developing brains. The NSP cells are also susceptible to CMV infection in adult and aged brains. The susceptibility can be enhanced by stimulation of neurogenesis. It was shown that latent murine CMV infection occurs in NSP cells by demonstrating the reactivation in brain slice culture or neurospheres. It is hypothesized that CMV brain disorder such as microcephaly is caused by disturbance of cellular events in the ventricular regions, including proliferation and differentiation of the neural stem cells, whereas neurons are also targets in persistent CMV infection, presumably resulting in functional disorders such as mental retardation.
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PMID:Roles of neural stem progenitor cells in cytomegalovirus infection of the brain in mouse models. 1842 23

Human cytomegalovirus (HCMV), a ubiquitous herpesvirus, is the main cause of congenital abnormalities and mental retardation in newborns and is also responsible for severe life-threatening complications in immunocompromised individuals, including AIDS patients and transplant recipients. The disorders generated by cytomegalovirus are closely associated with the competence of the host immune system and both humoral and cell-mediated mechanisms are involved in the response to viral infection. To identify viral proteins recognized by host antibody responses, a cytomegalovirus genome library was created and displayed on lambda bacteriophage. The challenge of such a library with sera from individuals with congenital or acquired infection allowed the identification of a wide panel of recombinant bacteriophages carrying cytomegalovirus B cell epitopes. Epitope-containing fragments within the families of tegument proteins (pUL25, pUL32), structural proteins (pUL48, pUL56) and glycoproteins (pUL55) were identified. Moreover, library screening permitted isolation of phage clones carrying an antigenic region of an uncharacterized HCMV protein encoded by the UL71 open reading frame (ORF), highlighting the potential of lambda display technology in antigen and epitope discovery.
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PMID:Molecular dissection of the human B cell response against cytomegalovirus infection by lambda display. 1849 73

Congenital cytomegalovirus (CMV) infection is the leading infectious cause of mental retardation and hearing loss in the developed world. In recent years, there has been an improved understanding of the epidemiology, pathogenesis, and long-term disabilities associated with CMV infection. In this review, current concepts regarding the pathogenesis of neurological injury caused by CMV infections acquired by the developing fetus are summarized. The pathogenesis of CMV-induced disabilities is considered in the context of the epidemiology of CMV infection in pregnant women and newborn infants, and the clinical manifestations of brain injury are reviewed. The prospects for intervention, including antiviral therapies and vaccines, are summarized. Priorities for future research are suggested to improve the understanding of this common and disabling illness of infancy.
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PMID:Neuropathogenesis of congenital cytomegalovirus infection: disease mechanisms and prospects for intervention. 1913 36

Cytomegalovirus (CMV) is the most common and serious congenital infection, because it occurs after both primary and recurrent infection in pregnancy and is a major cause of childhood deafness and neurological handicap. Fetal transmission generally occurs in 30-60% of women acquiring a primary infection or in 0.5-2% of women with preconceptional immunity. Following primary maternal infection, approximately one-third of the CMV-infected infants will have disease at birth or develop severe sequelae, which include convulsive or spastic syndromes, mental retardation and auditory and visual impairment. Routine antepartum and in pregnancy serological screening should be essential for avoiding doubtful interpretations of CMV-IgM results in pregnancy. Detection of quantitative CMV DNA in the amniotic fluid and accurate ultrasound examinations are needed in pregnant women with suspected primary infection. Being not yet available a vaccine and uncertain the results of postnatal ganciclovir therapy, CMV hyperimmunoglobulin appears to be the only safe and valid approach for prevention of congenital CMV disease.
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PMID:Maternal-fetal cytomegalovirus infection: from diagnosis to therapy. 1925 66

Primary cytomegalovirus (CMV) infection occurs during pregnancy in 1% to 4% of seronegative women and may be transmitted to the fetus in up to 40% of cases. Up to 10% of intrauterine CMV infections result in symptomatic congenital disease at birth. Half of these children and 13% of those born with asymptomatic infection will develop significant clinical sequelae in infancy, especially sensorineural hearing loss. Routine CMV screening during pregnancy is not recommended in Spain owing to the absence of an effective CMV vaccine, the lack of preventive measures or therapy during pregnancy, the difficulty in diagnosing a reactivated infection, and the possibility of symptomatic congenital infections in children of immune women. However, sensitive and specific methods to diagnose primary maternal and fetal infection now exist, and new preventive and therapeutic measures have been developed. Currently, these procedures are not universally available and need to be tested in larger trials. Furthermore, the prevalence of seropositive status in pregnant women, the frequency of congenital infection, and the percentage of infants born with hearing impairment and mental retardation in our country are not known. Therefore, it would not be appropriate to introduce routine screening for CMV in pregnancy at the present time. However, increased efforts should be made to inform women about congenital CMV disease, to develop the diagnosis of fetal infection and methods to determine the extent of involvement in the case of suggestive ultrasound findings, and to treat symptomatic infected newborns with antivirals to reduce hearing impairment.
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PMID:[Congenital cytomegalovirus infection: is serological screening during pregnancy necessary?]. 1940 63

Primary and recurrent infections of human cytomegalovirus (HCMV) can occur during pregnancy. Both can result congenital infection, the leading infectious cause of mental retardation, sensorineural deafness and visual impairment. Intrauterine transmission of HCMV and adverse outcome are mainly related to primary maternal infection. However, there is an increasing evidence that incidence of symptomatic infections in infants born to immune mothers is higher than previously thought. Therefore the option of prenatal diagnosis has a crucial role in the management of pregnancy complicated by active HCMV infection. In spite of the potentially devastating consequence of congenital HCMV infection, little information is available concerning antiviral therapy as prophylactic treatment for women at high risk of the transmission of HCMV during pregnancy. Passive immunization for prevention of vertical transmission of the virus seems to be promising. Until a HCMV vaccine is available, education regarding the risk and strategies for prevention of HCMV infection during pregnancy is needed.
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PMID:[Cytomegalovirus infection in pregnancy]. 1944 4

Congenital cytomegalovirus (CMV) infection is a significant cause of brain disorders, such as microcephaly, mental retardation, hearing loss and visual disorders in humans. The type and severity of brain disorder may be dependent on the stage of embryonic development when the congenital infection occurs. Developmental disorders may be associated with the type of embryonic cells to which CMV is susceptible and the effects of the infection on the cellular functions of these cells. Early murine embryos, including embryonic stem (ES) cells, are not susceptible to CMV infection. A part of the embryonic cells acquire susceptibility during early development. Mesenchymal cells are the targets of infection at midgestation, affecting organogenesis of the brain, eyes and oral-facial regions. In contrast to ES cells, neural stem progenitor cells (NSPC) from fetal brains are susceptible to murine CMV (MCMV) infection. The viral infection inhibits proliferation and differentiation of the NSPC to neuronal and glial cells in addition to induction of neuronal cell loss. These cellular events may cause brain malformations, such as microcephaly and polymicrogyria. Furthermore, MCMV persists in neuronal cells in developing brains, presumably resulting in neuronal dysfunction.
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PMID:Effects of cytomegalovirus infection on embryogenesis and brain development. 1948 54


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