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)

Acquired immunodeficiency virus infections had recently been the leading cause of death in minority women of reproductive age in several urban cities in the United States. In addition, more than 80% of infants with human immunodeficiency virus type 1 infection acquired the infection perinatally. These alarming data have spawned a prodigious body of information about perinatal human immunodeficiency virus type 1 infection. Some of the most recent advances are highlighted in this review. Revolutionary techniques, initially developed in molecular biology, such as in situ hybridization, the polymerase chain reaction, and gene sequencing, have also recently made a significant contribution to the diagnosis and better understanding of viral and bacterial infections. For example, organisms such as cytomegalovirus, herpes simplex, Chlamydia, parvovirus, Pneumocystis carinii, and toxoplasma are now detectable by polymerase chain reaction methods. The most recent information in these areas is also briefly reviewed.
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PMID:Maternal and fetal infections. 154 30

A patient who presented with pure red cell aplasia as the initial manifestation of human immunodeficiency infection is described. The patient had no signs of other autoimmune processes or immunologic or histologic evidence of parvovirus B19 infection, although we detected parvovirus B19 DNA in his serum. This patient had a complete, although temporary, response to a single course of immunoglobulin therapy and is currently responding to a second treatment.
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PMID:Red cell aplasia responsive to immunoglobulin therapy as initial manifestation of human immunodeficiency virus infection. 154 32

One hundred hemophilia A and 30 hemophilia B patients who had been treated with non-heated and heated factor VIII or prothrombin complex concentrates were examined by immunological tests including Clq-bearing immune complexes assay. Antibodies to human immunodeficiency virus type 1 (HIV-1), hepatitis B virus (HBV), hepatitis C virus (HCV) and human parvovirus B19 (B19) were analyzed by Western blotting, enzyme immunoassay, passive hemagglutination or radio-immunoassay. Clq-bearing immune complexes were assayed by a monoclonal anti-Clq ELISA system (Immunomedics). Seropositivity to HIV-1, HBV, HCV, and B19 was 56.9%, 87.7%, 79.2% and 100% respectively. Clq-bearing immune complexes were positive in 109 of the 130 patients (83.8%). The positivity and the levels were extremely higher than those in normal individuals. Clq-bearing immune complex levels in patient positive for HIV-1, HCV, or HBV were higher than those in the negative group (HIV: P less than 0.001, HCV: P less than 0.005, HBV: P less than 0.05). When the patients were divided into four groups according to seropositivity to HIV-1 and/or HCV, Clq-bearing immune complex levels were the highest in the group positive for both antibodies, and the lowest in the group negative for both antibodies. These results suggested that each viral infection influences the formation of immune complexes and repeated viral infection increased the level of Clq-bearing immune complexes in these patients.
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PMID:[Elevated Clq-bearing immune complexes in hemophiliacs with viral infections]. 177 53

In a female child with severe combined immunodeficiency, pure red cell aplasia was observed which required regular transfusions of erythrocytes. Parvovirus B 19 DNA (but no antibodies) was detected in stored serum samples after the death of the patient. We suggest that the anaemia was a consequence of parvovirus infection which persisted for at least 2 years due to the immunodeficiency.
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PMID:Persistence of parvovirus B19-DNA in blood of a child with severe combined immunodeficiency associated with chronic pure red cell aplasia. 191 97

Viruses have recently become appreciated as nosocomial pathogens. There is insufficient data to characterize trends in rates of viral nosocomial infections, but there have been major trends in methodologies and concepts. New groups of patients, such as infants and the elderly, are becoming appreciated as being at risk for serious nosocomial viral infections, whereas other groups, such as immunodeficient patients are expanding because of the epidemic of human immunodeficiency virus (HIV) infection and expanded use of immunosuppressive treatment. The continued addition of new viruses, such as HIV, human parvovirus B19, and rabies virus, to the list of potential nosocomial pathogens suggest that most human viruses can probably be serious nosocomial pathogens under the right circumstances. Advances in medical treatments and procedures, such as cadaveric dura mater grafts and laser treatment of warts, have provided new avenues for nosocomial transmission of viruses. Improved and wider availability of diagnostics promises to be a major force in improving our understanding and ability to prevent viral nosocomial infections. With these advances, viral diagnostic laboratories should become an important member of the infection control team. In parallel with trends in methodologies and concepts, there have been major advances in our understanding of ways to prevent some nosocomial viral infections. Application of these prevention measures is an important challenge to the infection control practitioner.
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PMID:Major trends in nosocomial viral infections. 192 51

Parvovirus B19 infection leads to transient aplastic crises in individuals with chronic hemolytic anemias or immunodeficiency states. An additional unexplained sequela of B19 infection is thrombocytopenia. Because B19 is known to have a remarkable tropism for human erythropoietic elements, and is not known to replicate in nonerythroid cells, the etiology of this thrombocytopenia is uncertain. We sought to define the pathobiology of B19-associated thrombocytopenia by examining the role of B19 on in vitro megakaryocytopoiesis. B19 infection of normal human bone marrow cells significantly suppressed megakaryocyte (MK) colony formation compared with mock-infected cells. No such inhibition was observed with a nonpathogenic human parvovirus, the adeno-associated virus 2 (AAV). The B19-MK cell interaction was also studied at the molecular level. Whereas low-density bone marrow cells containing erythroid precursor cells supported B19 DNA replication, no viral DNA replication was observed in B19-infected MK-enriched fractions as determined by the presence of viral DNA replicative intermediates on Southern blots. However, analysis of total cytoplasmic RNA isolated from B19-infected MK fractions showed a low-level expression of the B19 genome as detected by quantitative RNA dot blots as well as by Northern analysis. Furthermore, a frame-shift mutation in a recombinant AAV-B19 hybrid genome segment that encodes the viral nonstructural (NS1) protein significantly reduced the observed inhibition of MK colony formation. These studies indicate tissue-tropism of B19 beyond the erythroid progenitor cell, and lend support to the hypothesis that B19 genome expression may be toxic to cell populations that are nonpermissive for viral DNA replication.
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PMID:Parvovirus B19-induced perturbation of human megakaryocytopoiesis in vitro. 214 78

The prevalence of antibody to human parvovirus B19 was determined in 86 children with congenital bleeding disorders. Forty-seven of 53 boys (89%) receiving non-heat-treated factor VIII or prothrombin complex concentrates were anti-B19 IgG positive compared with 38% of their age-matched controls and 48% of children treated with cryoprecipitate. Acute B19 virus infection occurred in 2 boys 3-4 weeks after they had received the same batch of commercial factor VIII concentrate. Of 11 susceptible children who had only received heat-treated National Health Service factor VIII concentrate (8Y), 1 acquired anti-B19 IgG. This suggests that 8Y heat-treated concentrate has a much reduced risk of transmitting B19 virus and, by implication, other less heat-stable viruses such as human immunodeficiency virus.
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PMID:Transmission of human parvovirus B19 by coagulation factor concentrates. 216 Jan 47

A lambda gt11-random-primed-cDNA clone specific for chronic hepatitis C was isolated from pooled serum presumably infected by hepatitis C virus. The translation product of the clone detect 50% of patients with chronic hepatitis C in 4 test panels but none of the patients with acute hepatitis C, other liver diseases or normal controls was positive for the peptide. The nucleotide sequence of the cDNA clone, the size of which is 66 bp, has no homology to the complete sequences of known human viruses such as adenovirus, coxsackievirus, rhinovirus, immunodeficiency virus type 1, Epstein-Barr virus, polioma virus, poliovirus, papilloma virus, parvovirus, papovavirus, varicella-zoster virus, yellow fever virus, endogenous retrovirus, T-cell lymphotropic virus types I, II, and III Japanese encephalitis virus, and hepatitis A, B, and D viruses. Probably only one or two epitopes are present on the molecule encoded by the clone as the peptide consists of only 22 amino acid residues.
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PMID:A lambda gt11-cDNA clone specific for chronic hepatitis C generated from pooled serum presumably infected by hepatitis C virus. 250 79

B19 parvovirus is pathogenic in humans, causing the common childhood exanthem fifth disease and bone-marrow failure, both acute (transient aplastic crisis of hemolysis) and chronic (pure erythrocyte aplasia in immunodeficiency). The virus is tropic for a human red cell progenitor cell, and failure to culture B19 in a cell line has limited its clinical study. We cotransfected the right half of the cloned B19 genome and a minigene derived from the human dihydrofolate reductase gene (DHFR) into dhfr--Chinese hamster ovary cells and screened selected clones by RNA analysis; after amplification in methotrexate, clones were tested for capsid protein expression. A cell line, designated 3-11-5, stably expressed nearly full-length transcripts for the two capsid proteins. These cells produced the major and minor structural protein species in natural proportions that self-assembled into virion capsids. Capsids from 3-11-5 cells could be separated from virions by sucrose gradient sedimentation and had the density on cesium chloride isopycnic sedimentation of empty parvovirus capsids. Capsid protein was present in both nuclei and cytoplasm on immunofluorescence study but fractionated with the cytosol on purification. Empty capsid production was equal to or greater than virion production by infected bone-marrow cells, 1000-2000 capsids per cell, but cell growth was not diminished by capsid production. This cell line will be useful in developing practical assays for B19 parvovirus antibody and a vaccine for the virus, as well as potentially serving as a packaging cell line for gene therapy.
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PMID:A genetically engineered cell line that produces empty capsids of B19 (human) parvovirus. 267 9

The efficacy of two heating cycles (90 sec at 103 degrees C and 10 hr at 65 degrees C) used during manufacture of a plasma-derived hepatitis-B vaccine was validated for the inactivation of 12 virus families. A period of 15 min warming up to 65 degrees C had already completely inactivated representatives of nine virus families, ie, poxvirus (vaccinia), picornavirus (encephalomyocarditis virus), togavirus (sindbis virus), coronavirus (mouse hepatitis virus), orthomyxovirus (influenza virus), rhabdovirus (vesicular stomatitis virus), herpes virus (cytomegalovirus), lentivirus (human immunodeficiency virus), and retrovirus (murine leukemia virus). After prolonged heating at 65 degrees C or heating for 90 sec at 103 degrees C, parvovirus (canine parvovirus) and the phage phiX174 were also completely inactivated. Papovavirus represented by simian virus 40 (SV-40) was the most heat-resistant virus evaluated. The infectivity of SV-40 was reduced by 10(4) Tissue Culture Infectious Doses (TCID50) per ml after 90 sec at 103 degrees C, but a marginal residual activity (less than 1.5 TCID50 per ml) was observed. Subsequent pasteurization for 10 h at 65 degrees C did not further reduce the infectivity of SV-40. This study shows that the two heat-inactivation steps used during the production of this vaccine kill a wide variety of viruses that might be present in human blood.
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PMID:Inactivation of 12 viruses by heating steps applied during manufacture of a hepatitis B vaccine. 282 25


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