Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A slow influenzal congenital infection of man (in a child aged 2.5 years) is described for the first time. The infection manifests itself by encephalomyelopathy (retarded psychomotor development, sluggish spinal pareses of the limbs) and resembles Werdnig-Hoffmann amyotrophy. Besides, one can ses neuroendocrine disorders (hypophyseal nanism, hypogonadism ) and the signs of immunodeficiency. The long-term persistence of influenza A virus, its defective form was detected in the blood and CSF by means of molecular hybridization. In addition, the summarized data on the clinical studies of congenital influenzal injuries to the CNS in children, carried out by the author are provided. The theoretical evidence for the work was experimental slow influenzal infection in mice obtained for the first time at the N.F.Gamaleia Institute of Epidemiology and Microbiology (Moscow).
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PMID:[Congenital encephalomyelopathy as a possible slow infection in humans]. 164 19

A malformation syndrome has been proposed in infants with acquired immunodeficiency syndrome or acquired immunodeficiency syndrome-related complex secondary to congenital infection with human immunodeficiency virus (HIV) in the United States and Europe. To determine whether embryopathy is detectable in HIV-exposed African infants, 85 infants of HIV-seropositive mothers and 98 infants of HIV-seronegative mothers in Nairobi, Kenya, were examined for minor and major anomalous features shortly after birth. No mother used intravenous drugs. With the exception of growth failure no anomalous feature was associated with in utero HIV exposure. No increase in the number of anomalous features per infant was correlated with HIV, nor did any infant have the reported malformation syndrome. Thus in this population of African infants examination for anomalous features during the neonatal period failed to identify those infants with fetal exposure to HIV.
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PMID:Lack of correlation of maternal human immunodeficiency virus infection with neonatal malformations. 281 15

Congenital infection is uncommon and the cause of only a small proportion of handicap seen in children but some infections may be preventable or even treatable. As an example, the congenital rubella syndrome first described in the 1940s is preventable by use of the vaccine but cases still occur. It is hoped that with the introduction of the measles, mumps, rubella immunization for young children, rubella will become as rare in the UK as it is in the USA. Cytomegalovirus is now a more common cause of handicap than rubella but no vaccine has been developed. Although antiviral drugs are available for herpes simplex virus and vaccinia, infection mortality in the newborn is high, even following the use of these agents; many HSV infections in the newborn arise following primary and asymptomatic maternal infections so that treatment may start late in the course of the illness. The obstetrician needs to understand the natural history as well as possible investigations available for congenital infections. There may be warning signs which require action, such as herpetic lesions in the genital tract of the mother. Less specific abnormalities during pregnancy, such as intra-uterine growth retardation and spontaneous onset of preterm labour, may point to congenital infection. This chapter describes both antenatal and postnatal management of the major congenital infections. We have included recent research data that should influence clinical practice; studies on HSV which suggest that, for women with a history of recurrent infection, routine viral culture of the genital tract at the end of pregnancy is unnecessary; reports from both the USA and the UK that rubella immunization performed inadvertently during early pregnancy has not resulted in the congenital rubella syndrome. The chapter would not have been complete without a discussion of human immunodeficiency virus, of concern to the obstetrician and midwife. There is still much to be learned about the natural history of this infection in both the mother and infant.
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PMID:Infection of the fetus and the newborn: prevention, treatment and related handicap. 284 13

This is the second of two articles summarizing the information currently available on herpes virus diseases. The first described the different members of the herpesvirus group, clinical expression of infection, laboratory diagnosis, and chemotherapy. This article dealing with the epidemiological and immunological aspects of herpesvirus infections also brings up the special problems caused by virus latency and risks associated with congenital infection and immunodeficiency or immunodepressive treatment. The prospects of preventing herpesvirus infections by vaccination and treatment with immune sera are also discussed.
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PMID:Prevention and control of herpesvirus diseases. Part 2. Epidemiology and immunology. 299 97

The causative agent of acquired immunodeficiency syndrome is a retrovirus, human T lymphotropic virus type III/lymphadenopathy-associated virus, now known as human immunodeficiency virus (HIV). Infection of children with HIV results in a wide spectrum of clinical manifestations, ranging from asymptomatic to symptomatic, with the severest disease forms including neurologic deterioration, opportunistic infections and malignancy. This virus infects preferentially T cells bearing the CD4 receptors and also seems to exhibit preference for the central nervous system. The predominant route of infection in children is transplacental, and most affected children are infected at the time of birth. For women who give birth to infants with congenital infection with HIV, the main risk factor is intravenous drug abuse; a smaller percentage of these women acquire the infection via sexual contact and a few are infected via blood transfusions. Estimates for the incidence of transmission of the virus from an infected mother to her offspring vary from about 20 to 70%. Infection in most children and adults is documented by serologic testing, inasmuch as almost all infected people are HIV antibody-positive. Mothers of congenitally affected children are always HIV antibody-positive and also frequently have immune abnormalities. Women who give birth to infected children may, however, be asymptomatic in 50% of instances or more. Because antibodies to HIV are predominantly of the IgG class, they cross the placenta. All infants born to infected women therefore acquire passively transferred antibodies to HIV irrespective of whether or not the infants are infected with the virus itself. These passively transferred antibodies may sometimes persist for as long as 15 months. Thus in infants and children under 15 months of age in the absence of symptoms, the only definitive way to establish diagnosis is by viral isolation or viral antigen detection. Clinically the HIV-infected children can be divided into two groups, symptomatic and asymptomatic. Among the symptomatic group the main diagnostic specific features are: (1) opportunistic infection, e.g. with Pneumocystis carinii pneumonia; (2) interstitial pneumonitis with respiratory distress resulting from lymphocytic interstitial pneumonitis; (3) microcephaly and other neurologic abnormalities; (4) recurrent bacterial infections.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Human immunodeficiency virus infection in children: nature of immunodeficiency, clinical spectrum and management. 304 60

Human herpesvirus 6 (HHV-6), an important opportunistic pathogen in immunocompromised patients, causes fatal pneumonitis, encephalitis, and bone marrow suppression. Its ability to infect and destroy T lymphocytes may allow it to synergize with the human immunodeficiency virus in the destruction of lymphoid tissues in patients with AIDS. We describe herein an infant who had an immunodeficiency associated with thymic atrophy and severe T lymphocytopenia who developed fatal pneumonitis due to HHV-6. Dense and disseminated infection of T lymphocytes with HHV-6 was also documented. In the absence of any other documented cause of immunodeficiency, we hypothesize that congenital infection of this infant with HHV-6 may have caused progressive destruction of her cellular immune system, leading to the fatal pneumonitis. Thus, HHV-6 infection may have been the cause of both her immunodeficiency and her fatal opportunistic infection.
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PMID:Progressive immunodeficiency and fatal pneumonitis associated with human herpesvirus 6 infection in an infant. 774 49

Information on congenital infection is continuously expanding. New diagnostic techniques are making significant contributions to the prenatal diagnosis of several fetal infections. In this review we highlight some of the most recent advances in the diagnosis and management of the most common fetal infections, those caused by cytomegalovirus, human immunodeficiency virus 1, Toxoplasma, varicella-zoster virus, and parvovirus B19.
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PMID:Management strategies for congenital infections. 779 74

Although the mechanisms for maternal transmission are unknown, approximately half of the infants congenitally infected with the human immunodeficiency virus type 1 (HIV-1) seem to become infected late in gestation or during delivery. Previously, we have developed a rhesus monkey model for congenital infection by injecting cell-free simian immunodeficiency virus (SIV) directly into amniotic fluid. Our results suggested that fetal infection may have occurred via skin or mucous membrane exposure. Mucosal surfaces have also been implicated as a portal of virus entry by a study in which the presence of serosanguinous fluid in neonatal gastric aspirates correlated with an increased rate of HIV-1 transmission. To test whether cell-free virus could transverse intact neonatal mucosal surfaces, we administered SIVmac251 orally to four rhesus monkey neonates within 1 hr following cesarean section delivery. All four neonates developed viremia and were positive by cocultivation and PCR. Seroconversion occurred in three of the four neonates. The SIV dose given was within physiological range as shown by end-point dilution of virus stock and viremic plasma samples of juvenile rhesus monkeys. This primate model for mucosal transmission of cell-free virus features a high infection rate, thus making studies of mucosal immunity and the development of strategies to prevent intrapartum virus transmission possible.
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PMID:Mucosal infection of neonatal rhesus monkeys with cell-free SIV. 806 15

Pregnant women are exposed to many biological, eg microbial, agents, which are potentially harmful to the fetus. The reported rates of vertical transmission of hepatitis B and human immunodeficiency virus vary between 3 to 90% and 0 to 65%, respectively. The susceptibility to hepatitis B and human immunodeficiency infection is increased in pregnant physicians, midwives, and nurses because of the bloodborne nature of these viruses. Also, TORCH (toxoplasmosis-rubella-cytomegalovirus-herpes) infections, acquired during pregnancy, may result in congenital infection, and serious sequelae in the neonatal period or years after birth. Schoolteachers and daycare personnel have an increased risk of perinatal varicella, "fifth disease," and mumps. Perinatal listeriosis affects one in 20,000 births and may result in fetal wastage. Because of the risk of the possibility of vertical transmission, immunization during pregnancy with live virus vaccines is not recommended.
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PMID:Biological agents and pregnancy. 852 Sep 61

We report on two children who may represent a novel syndrome consisting of a deficiency of immunoglobulin-bearing B lymphocytes and serum antibody, deficient intrauterine and/or postnatal growth, intracranial calcifications, and acquired pancytopenia. Poor growth, intracranial calcifications, developmental delay, and hematological abnormalities are common manifestations of congenital infection. However, humoral immunodeficiency is not characteristic in these infections, and no infection was found on extensive evaluation. Rare genetic syndromes may mimic intrauterine infections and may also include immunodeficiency. However the children reported here lack important characteristics or share distinctive manifestations not described in these disorders. Infants presenting with apparent congenital infections in whom a specific infectious cause cannot be identified should be followed carefully with immunological evaluations since this disorder may be progressive and considerable morbidity is attributable to hematological and immunological manifestations.
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PMID:Growth failure, intracranial calcifications, acquired pancytopenia, and unusual humoral immunodeficiency: a genetic syndrome? 1107 89


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