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)

Five strains of human immunodeficiency virus type 1 (HIV-1) were isolated from five Japanese hemophilia patients. Two isolates, HIV-1[GUN-1] and HIV-1[GUN-2], were from brother patients with hemophilia B and the other three isolates, HIV-1[GUN-3], HIV-1[GUN-4], and HIV-1[GUN-5], were from hemophilia A patients. Another HIV-1 strain, HIV-1[GUN-6], was isolated from a Canadian male homosexual with AIDS. The restriction endonuclease cleavage maps of the proviral genomes of these six HIV-1 strains revealed that they were apparently different from each other. The phylogenetic trees constructed using restriction maps and nucleotide sequences were quite similar, indicating that phylogenetic analyses of Japanese HIV-1 isolates can be done using restriction maps of the proviruses. Phylogenetic analyses showed that they were more closely related to HIV-1s which had been reported to be isolated from homosexual patients in the United States than those isolated from African patients. In particular, GUN-1 and GUN-2 isolates were on the branch of a San Francisco isolate, ARV2, while GUN-5 and GUN-6 isolates were on the branch of HTLV-IIIB-related isolates.
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PMID:Six strains of human immunodeficiency virus type 1 isolated in Japan and their molecular phylogeny. 140 18

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

Two hundred and eighty-two patients with congenital bleeding disorders received blood component replacement therapy between January 1979 and April 1985, were followed-up by the Puget Sound Blood Center's Hemophilia Care Program, and were tested for antibody to human immunodeficiency virus (HIV). Serologic results were obtained at least 1 year after the last exposure to volunteer donor products that were prepared before donor HIV screening or after the last exposure to concentrates produced before the manufacturer's use of treatment methods for inactivation of HIV. In all, 106 patients were anti-HIV positive. The risk of HIV infection was greater in patients with more severe bleeding tendencies, greater exposure to components, and exposure to lyophilized concentrates from large pools of donors. Of 100 patients with hemophilia A who only received cryoprecipitate from volunteer donors from Washington State (during the 6.3-year period), 14% had become anti-HIV positive. Of 27 patients receiving mostly cryoprecipitate but also being exposed to a single lot of concentrate during the same period, 13 (48%) were positive. Of 49 patients treated predominantly or solely with factor VIII concentrates during this period, 43 (88%) were anti-HIV positive. Of 29 patients with von Willebrand disease, four were anti-HIV positive, including 2 of 26 receiving only cryoprecipitate and two of three who had received a single dose of factor VIII concentrate. Of 19 patients who were treated solely with volunteer donor plasma, all remained anti-HIV negative. Of 47 patients exposed to factor IX concentrate, 28 (60%) were positive. Data relevant to the risk of HIV transmission subsequent to screening of the volunteer donor population were also obtained. Treatment records of 55 hemophilia A patients who have remained anti-HIV negative through at least June 1990 showed exposure to 71,173 screened donors from May 1985 through December 1989, and all 55 patients have remained anti-HIV negative.
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PMID:Treatment type and amount influenced human immunodeficiency virus seroprevalence of patients with congenital bleeding disorders. 188 29

As part of a prospective cohort study initiated in 1983, the human immunodeficiency virus type 1 (HIV-1) status has been periodically determined for patients with clotting disorders (hemophilia A or B, von Willebrand's disease, miscellaneous). The University of North Carolina Hospitals has conducted comprehensive surveillance for nosocomial infections (NI) using modified Centers for Disease Control criteria since 1980 and entered this information in a computerized data base. Cross-matching of our NI data base and hemophiliac/HIV-1 study data base for the time period 1980-1989 revealed that 13 NI occurred in 11 patients during 659 hospitalizations (5,723 hospital days). NI rates per 100 admissions (per 1,000 hospital days) by HIV-1 status were as follows: HIV-1 negative = 0.91 (1.18), HIV-1 positive pre-AIDS = 1.65 (1.84), and AIDS = 6.67 (6.48). NI occurred with a similar frequency in HIV-1 positive pre-AIDS hemophiliacs and HIV-1 negative hemophiliacs (Fisher's exact test, p greater than 0.10). However, NI occurred more frequently in hemophiliacs with AIDS versus HIV-1 positive or negative hemophiliacs (Fisher's exact test, p less than 0.05). We conclude that HIV-1 infection does not appreciably alter the risk of developing a NI, but that patients who have progressed to AIDS are at significantly increased risk of developing a NI per hospital day or per hospitalization.
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PMID:Nosocomial infection rate as a function of human immunodeficiency virus type 1 status in hemophiliacs. 192 66

We have studied the conditions of in vitro binding of platelet glycoprotein IIb/IIIa (GPIIb/IIIa) to fibrinogen and applied the results to identify and measure the serum inhibitors to the binding. For the enzyme-linked immunosorbent assay, platelet extract was delivered to a fibrinogen-coated microtiter plate that was incubated for 2 hours, followed by incubation with anti-GPIIb/IIIa monoclonal antibody for another 2 hours. The plate was then incubated with peroxidase-conjugated anti-mouse IgG for color development. The binding was shown to be calcium-dependent. The binding was partially blocked by treating the coated fibrinogen with anti-fibrinogen antibody. Reduction or dissociation of GPIIb/IIIa resulted in the total loss of its ability to bind to fibrinogen. Platelet extracts of patients with hemophilia showed decreased binding (25% and 14%, compared with control platelet extract), and an extract from a patient with Glanzmann's thrombasthenia showed no binding. With the enzyme-linked immunosorbent assay we have measured serum inhibitors to GPIIb/IIIa binding to fibrinogen in 35 hemophilia A, 17 immune thrombocytopenic purpura, 22 human immunodeficiency virus-related immune thrombocytopenic purpura, and 29 systemic lupus erythematosus serum samples. In those patients with inhibition by serum, polyethylene glycol precipitation of circulating immune complexes (CICs) decreased the inhibition by the supernatants, and all the resolubilized CIC precipitates demonstrated inhibition, which indicates that CICs play a major role in the inhibition of GPIIb/IIIa binding to fibrinogen. This, then, provides evidence of CIC-mediated impaired GPIIb/IIIa binding to fibrinogen in hemophilia A, HIV-ITP, and SLE.
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PMID:Inhibition of platelet GPIIb/IIIa binding to fibrinogen by serum factors: studies of circulating immune complexes and platelet antibodies in patients with hemophilia, immune thrombocytopenic purpura, human immunodeficiency virus-related immune thrombocytopenic purpura, and systemic lupus erythematosus. 200 77

Six patients with Hodgkin's disease (HD) and demonstrable serum antibodies to human immunodeficiency virus (HIV) and two additional patients with HD belonging to HIV-associated high-risk groups but with negative HIV serology were studied. All patients were men and ranged in age from 21 to 45 years. The HIV risk factors included homosexuality (6), intravenous drug abuse (2), and hemophilia A (1). All patients had high pathologically determined stage (one Stage III and seven Stage IV), and bone marrow involvement was observed in five patients with the initial diagnosis of HD based on marrow biopsy in two cases. Four cases were histologically subclassified as mixed cellularity (MC) and three as nodular sclerosis (NS); one patient underwent only bone marrow biopsy and was not subclassified. Histologically all cases were characterized by numerous Reed-Sternberg cells and variants, and with the exception of one case, all had a distinctive decrease in the proportion of reactive background lymphocytes compared with what is usually expected in MC or NS Hodgkin's disease (relative lymphocyte depletion). Flow-cytometric immunophenotypic studies done on cell suspensions from diagnostic lymph node biopsies in four cases showed decreased CD4:CD8 ratios (mean = 1.4) compared with expected values of 4 to 6. The relative lymphocyte depletion observed histologically is probably a reflection of the decreased tissue CD4:CD8 ratios, and this impairment of host immune response may be related to the observed high stage in all eight cases. Patients with high stage HD and the described histologic and immunologic features should be evaluated for the presence of HIV infection.
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PMID:Hodgkin's disease in association with human immunodeficiency virus infection. Pathologic and immunologic features. 200

Intravenous administration of a high dose of intact-immunoglobulin to a human immunodeficiency virus (HIV) infected patient with hemophilia A, whose total lymphocyte and CD4 positive lymphocyte counts showed a decreasing tendency, resulted in a gradual rise in these cell counts. The results were quite reproducible on another occasions. Therefore, intravenous administration of gammaglobulin (IVGG) was thought to be effective for preventing further deterioration of cellular immunity and progression from asymptomatic carrier (AC) to AIDS related complex (ARC)/AIDS in hemophilia patients.
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PMID:High dose intact-immunoglobulin treatment for an HIV-infected asymptomatic carrier with hemophilia. 210 3

Thirteen hemophilia centers provide comprehensive care to approximately 90 percent of persons with hemophilia in California. For 1987, these centers reported patient human immunodeficiency virus (HIV) antibody status, age group, level of clotting factor deficiency, and hemophilia type on 1,438 persons with hemophilia A and B; HIV serologic status was known for 860 persons (59.8 percent) of whom 537 (62.4 percent) were HIV-antibody-positive. The HIV positivity rate increased with age after taking into account hemophilia type, clotting factor level and treatment center type. The three-year cumulative incidence of reported AIDS (acquired immunodeficiency syndrome) cases based on the number of HIV positive patients, was 11.6 percent. The cumulative incidence rate was 14.6 percent (54 of 370) for those patients over 20 years of age and 4.8 percent (8 of 167) for those under 21 years of age. Although a comparable distribution of the date of diagnoses of AIDS was seen by age group, there appeared to be a bimodal distribution in the rate of AIDS among the age groups, with the 6-12-year-olds and the 21 and older age groups showing higher incidence rates.
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PMID:Age and human immunodeficiency virus infection in persons with hemophilia in California. 211 1

The treatment of hemophilia A patients has progressed in the last 30 years. The development of more pure factor VIII concentrates has been encouraged by the appearance of the human immunodeficiency virus in blood supply. Monoclate was the first essentially pure form of factor VIII available for hemophilia therapy. The liquid pasteurized form of Monoclate represents a new standard for therapy that attempts to eliminate a broad spectrum of viral content in factor VIII preparations.
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PMID:Preclinical characterization of a new pasteurized monoclonal antibody purified factor VIIIC. 212 54

The treatment of plasma with organic solvent/detergent mixtures at the time of plasma collection or pooling could reduce the exposure of technical staff to infectious viruses and enhance the viral safety of the final product. Treatment of plasma for 4 hours with 2-percent tri(n-butyl)phosphate (TNBP) at 37 degrees C, with 1-percent TNBP and 1-percent polyoxyethylensorbitan monooleate (Tween 80) at 30 degrees C, or with 1-percent TNBP and 1-percent polyoxyethylene ethers, (Triton X-45) at 30 degrees C resulted in the rapid and complete inactivation of greater than or equal to 10(4) tissue culture-infectious doses (TCID50) of vesicular stomatitis and Sindbis viruses, which are used as surrogates. Treatment of plasma with TNBP and TNBP and Tween-80 was shown to inactivate greater than or equal to 10(4) TCID50 of human immunodeficiency virus. TNBP treatment of plasma contaminated with 10(6) chimpanzee-infectious doses (CID50) of hepatitis B virus and 10(5) CID50 of non-A,non-B hepatitis virus prevented the transmission of hepatitis to chimpanzees. Immediately after treatment of plasma with 2-percent TNBP, the recovery of factors VIII, IX, and V and antithrombin III was 80, 90, 40, and 100 percent, respectively. Recovery of all factors was greater than or equal to 90 percent after treatment with TNBP and detergent mixtures. Treated plasma was fractionated by standard techniques into antihemophilic factor and prothrombin complex concentrates, immune globulin, and albumin. Prior treatment with TNBP or TNBP and detergent did not affect the separations of desired proteins. Therefore, it appears possible to inactivate viruses in plasma before the execution of standard fractionation procedures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The use of tri(n-butyl)phosphate detergent mixtures to inactivate hepatitis viruses and human immunodeficiency virus in plasma and plasma's subsequent fractionation. 175 94


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