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

Human cytomegalovirus (CMV) infection can be life threatening in the immune compromised and is associated with congenital defects and / or mental retardation in the neonate. The demonstrated association between CMV infection and rheumatoid factor (RF) raised the possibility of an induction of an autoimmune response upon vaccination with a candidate CMV vaccine, glycoprotein gB (UL55). The antibody responses generated after injections of an adenovirus-gB construct (Ad-gB) were studied in autoimmune-prone (MRL/mpj) and normal (BALB.k, C3H, and BALB/c) mice. Enzyme-linked immunosorbent assay and immunoblot analyses were done to identify the autoantibodies produced following immunization. Immunization with Ad-gB induced a significant IgG anti-viral response in all strains tested (p < 0.0001) compared to phosphate-buffered saline or HeLa controls. Ad-gB induced a significant IgG autoantibody response (p > 0.005) to the U1-70 kDa spliceosome protein in both autoimmune and normal strains whereas immunization with recombinant human La/SS-B did not. Autoantibodies to U1-70 kDa are part of the anti-ribonucleoprotein response seen in systemic lupus erythematosus and mixed connective tissue disease. Low levels of IgG RF and anti-double-stranded DNA antibodies were also induced. This study raises concern that immunization with CMV gB in individuals genetically predisposed to autoimmunity could trigger the development or acceleration of an autoimmune disease.
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PMID:Recombinant cytomegalovirus glycoprotein gB (UL55) induces an autoantibody response to the U1-70 kDa small nuclear ribonucleoprotein. 1055 20

Congenital cytomegalovirus (CMV) infection is the leading infectious cause of mental retardation in children. Using seroprevalence data from two large antenatal populations (in excess of 14000 women) coupled with a mathematical modelling approach, we have shown that CMV has a low force of infection (ca. 0.03 per seronegative per annum) and its basic reproductive number R0 is relatively modest at 2.4. On the basis of these results, the critical vaccination proportion required for eradication of CMV is between 59-62%. In contrast to the predicted and observed effects of rubella vaccination on the incidence of congenital rubella, the increase in the average age of infection following instigation of a CMV vaccine programme will not increase the number of congenital infections. In conclusion, CMV is a prime candidate for eradication from the human population through vaccination.
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PMID:Encouraging prospects for immunisation against primary cytomegalovirus infection. 1116 56

This study was carried out to determine the prevalence of cytomegalovirus (CMV) excretion in urine among 30 deaf children and 91 mentally retarded children by cell culture and PCR. As a control, urine samples from 121 children without hearing disability or mental retardation were also tested. The study revealed that 15 of 30 (50%) deaf children and 16 of 91 (17.6%) mentally retarded children were excreting CMV in their urine. Among the control group we observed that only 2 of the 121 (1.8%) children were CMV excretors. As CMV excretion in urine is generally considered to indicate a congenital infection, it is very likely that congenital CMV is highly incriminated in mental retardation and deafness among children in Mauritius.
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PMID:Detection of cytomegalovirus in urine of hearing-impaired and mentally retarded children by PCR and cell culture. 2133 93

Like varicella zoster virus (VZV), human cytomegalovirus (HCMV) causes disease after both primary and recurrent infections. The former is more serious, particularly in pregnant women, who may transmit the virus to their offspring, with a high risk of mental retardation and deafness. Various experimental vaccines are in development, ranging from live, attenuated HCMV, subunit envelope glycoprotein, poxvirus vectors with CMV genes inserted, and plasmid DANN.
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PMID:Vaccination against cytomegalovirus. 1133 41

We report two cases of a peculiar leukoencephalopathy with temporal cysts. Both patients have a non-progressive neurological disorder with mental retardation, microcephaly and sensorineural deafness although clinical differences between them may reflect a different aetiology. The metabolic disorders with white matter involvement and the recently described leukoencephalopathies (Van Der Knaap disease, 'vanishing white matter disease') were excluded based on clinical, biologic and imaging findings. Cytomegalovirus infection is a likely possibility in the first case although the magnetic resonance imaging picture is only partially similar to previously reported cases. Our patients are strikingly similar to the patients reported by Deonna et al. and Olivier et al. We discuss the clinical and imaging findings in our patients and the differential diagnosis considering the known disorders of the white matter in childhood.
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PMID:Non-progressive leukoencephalopathy with bilateral temporal cysts. 1158 66

Cytomegalovirus (CMV), a member of the herpes virus family, is the most common cause of congenital infection in humans, affecting 0.5-3% of all newborns worldwide. Congenital cytomegalovirus infection is the leading infectious cause of deafness, learning disabilities, and mental retardation in children. The high prevalence of cytomegalovirus in the general population, unpredictability of transmission, and asymptomatic nature of the disease in otherwise healthy women challenge prevention and treatment efforts.
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PMID:Cytomegalovirus infection: perinatal implications. 1184 23

Human cytomegalovirus (HCMV) is the leading cause of congenital viral infection and mental retardation. HCMV infection, while causing asymptomatic infections in most immunocompetent subjects, can be transmitted during pregnancy from the mother with primary (and also recurrent) infection to the fetus. Hence, careful diagnosis of primary infection is required in the pregnant woman based on the most sensitive serologic assays (immunoglobulin M [IgM] and IgG avidity assays) and conventional virologic and molecular procedures for virus detection in blood. Maternal prognostic markers of fetal infection are still under investigation. If primary infection is diagnosed in a timely manner, prenatal diagnosis can be offered, including the search for virus and virus components in fetal blood and amniotic fluid, with fetal prognostic markers of HCMV disease still to be defined. However, the final step for definite diagnosis of congenital HCMV infection is detection of virus in the blood or urine in the first 1 to 2 weeks of life. To date, treatment of congenital infection with antiviral drugs is only palliative both prior to and after birth, whereas the only efficacious preventive measure seems to be the development of a safe and immunogenic vaccine, including recombinant, subunit, DNA, and peptide-based vaccines now under investigation. The following controversial issues are discussed in the light of the most recent advances in the field: the actual perception of the problem; universal serologic screening before pregnancy; the impact of correct counseling on decision making by the couple involved; the role of prenatal diagnosis in ascertaining transmission of virus to the fetus; the impact of preconceptional and periconceptional infections on the prevalence of congenital infection; and the prevalence of congenitally infected babies born to mothers who were immune prior to pregnancy compared to the number born to mothers undergoing primary infection during pregnancy.
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PMID:Diagnosis and management of human cytomegalovirus infection in the mother, fetus, and newborn infant. 1236 75

Congenital cytomegalovirus (CMV) infection is a major cause of sensorineural hearing loss and mental retardation, whose annual healthcare costs in the USA approximate to one billion dollars. Only a minority of neonates with this infection has symptoms present at birth and some of the damage to ear and brain occurs in the first few months of life. Extensive studies of CMV infection have been conducted in pregnant women and their children to define the natural history of this infection. What is required now is a concerted commitment to tackle this clinical problem using one or more of the following strategies: avoid iatrogenic transmission; advise those at risk how to avoid acquisition; provide diagnosis in an individual neonate or pregnant woman and offer treatment; develop and deploy a CMV vaccine.
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PMID:Strategies to prevent CMV infection in the neonate. 1240 Dec 99

Specific IgG antibodies against Toxoplasma, rubella, cytomegalovirus and herpes simplex (TORCH agents) were investigated in 32 infants and children with unexplained mental retardation (MR) and their mothers. 16 mentally normal infants and children of the same age group and their mothers were chosen as controls. Specific Toxoplasma IgG antibodies were 43.75% for MR cases and 37.5% for their mothers. Six (18.75%) mothers gave history of eating raw meat and canned food, while 8 (25%) had pet cats. 56.25% of the MR cases, and 81.25% of their mothers were positive to specific rubella IgG antibodies. 75% of MR cases and 81.25% of their mothers were positive for CMV specific IgG antibodies. Also, 18.75% of the MR cases and 25% of their mothers showed positivity to herpes simplex specific IgG antibodies. 93.75% showed positivity to one or more of the mentioned pathogenic agents.
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PMID:Studies on prenatal infections in children with unknown cause of mental retardation and examination of their mothers. 1256 83

Human cytomegalovirus (HCMV), a ubiquitous herpesvirus, causes a lifelong subclinical infection in healthy adults but leads to significant morbidity and mortality in neonates and immunocompromised individuals. Its ability to grow in different cell types is responsible for HCMV-associated diseases, including mental retardation and retinitis, and vascular disorders. To globally assess viral gene function for replication in cells, we determined the genomic sequence of a bacterial artificial chromosome (BAC)-based clone of HCMV Towne strain and used this information to delete each of its 162 unique ORFs and generate a collection of viral mutants. The growth of these mutants in different cultured cells was examined to systematically investigate the necessity of each ORF for replication. Our results showed that 45 ORFs are essential for viral replication in fibroblasts and 117 are nonessential. Some genes were found to be required for viral replication in retinal pigment epithelial cells and microvascular endothelial cells, but not in fibroblasts, indicating their role as tropism factors. Interestingly, several viral mutants grew 10- to 500-fold better than the parental strain in different cell types, suggesting that the deleted ORFs encode replication temperance or repressing functions. Thus, HCMV encodes supportive and suppressive growth regulators for optimizing its replication in human fibroblasts, epithelial, and endothelial cells. Suppression of viral replication by virus-encoded temperance factors represents a novel mechanism for regulating the growth of an animal virus, and may contribute to HCMV's optimal infection of different tissues and successful proliferation among the human population.
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PMID:Functional profiling of a human cytomegalovirus genome. 1462 81


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