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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

B19 infection offers some general lessons about human viruses and their possible effects on the human host, as follows: (1) Ubiquitous apparently benign viruses may have severe effects on a compromised host. The virus may be invariable but the host can have diverse susceptibilities. (2) B19 and some other human viruses (though for none is the evidence so clear as for B19) have narrowly targetted effects. The host cell of B19 is a specialised progenitor of mature red cells: impairment of the function of this cell by B19 may cause profound anaemia. (3) The 'normal' host response to B19 may also cause disease, though this is self limiting. (4) The effects of malfunction of the virus' target cell are exacerbated when the immune response is impaired by congenital or acquired immunodeficiency, immunosuppressive therapy or, in the case of the fetus, developmental immaturity that allows the virus to persist.
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PMID:Human B19 parvovirus infection: an example of multiple pathogenic effects determined by differences in host susceptibility. 134 9

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

Many agents are associated with bone marrow failure, including toxins, inherited metabolic defects, ionizing radiation, and viral infection. In most cases, the etiologic agent is unknown. Many of these unclassified cases have symptomatic, immunologic, or epidemiologic similarities to viral infections. Viruses from different taxonomic families have been implicated in bone marrow failure syndromes, and they appear to cause hematosuppression by a variety of mechanisms. Some of the viruses involved in relatively well characterized suppressive interactions will be reviewed, including parovovirus B19, dengue, hepatitis viruses, Epstein-Barr virus, cytomegalovirus and the human immunodeficiency virus.
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PMID:Viruses and bone marrow failure. 165 29

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

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

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

Chronic B19 parvovirus infection in patients infected with human immunodeficiency virus type 1 (HIV-1) is one cause of reversible anemia in this patient group. This report describes a case of concurrent HIV-1 and B19 parvovirus infection with pure red cell aplasia in which the anemia resolved with gammaglobulin treatment. When cultured in vitro with recombinant human stem cell factor, the red blood cell precursors from this patient demonstrated increases in both number and size, suggesting that simultaneous infection with B19 parvovirus and HIV-1 does not preclude a response to erythroid-acting growth factors. Although rare, persistent B19 parvovirus infection has become an increasingly recognized treatable cause of anemia in HIV-infected patients. Further in vitro and in vivo studies are required to determine whether cytokines such as stem cell factor have a consistent effect in these anemic states.
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PMID:In vitro erythroid effects of human stem cell factor in a case of human immunodeficiency virus-related chronic parvovirus B19 induced anemia. 768 13

Since some haemophiliacs manifest profound immunodeficiency with no evidence of human immunodeficiency virus type 1 (HIV) infection, we measured the circulating immune complex (CIC) level in sera obtained from haemophiliacs and addressed the question of whether viral infection is associated directly or indirectly with enhanced CIC production. While more than 90% of HIV-positive individuals had a high level of CIC, around 60% of seronegative ones also showed CIC levels comparable to those of seropositive patients. These sera activated fresh complement in vitro. The patients infected with either HIV or Hepatitis C virus (HCV) or both showed higher frequency and concentration of serum CIC than those free of either pathogens. It is worth noting, however, that 64% of patients with no evidence of infection with HIV or HCV produced significant amounts of CIC. Among the infectious viruses examined, parvovirus is considered as one of the pathogens associated with CIC synthesis, since all the haemophiliacs including the HIV-free patients who had been supplied with heated coagulation factors for several years from birth carried antibodies to parvovirus B19. Strikingly, 60% of the children in this category were positive for CIC, suggesting the possible contribution of parvovirus infection to CIC formation.
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PMID:Immunological abnormalities in HIV-free haemophiliacs. 770 43


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