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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with the acquired immunodeficiency syndrome (AIDS) suffer from a deficiency of cellular immunity. However, some HIV-infected children and adults suffer from recurrent upper respiratory tract infections suggestive of a failure to synthesise specific antibodies, despite the hypergammaglobulinaemia that is present. Intravenous immunoglobulin (IV IgG) appears to benefit HIV-infected children with recurrent infections, in doses similar to those used for treating patients with primary hypogammaglobulinaemia. In some HIV-infected adults, IV IgG also appears to reduce bacterial respiratory infections but the treatment schedules remain to be defined. In patients with life-threatening bleeding due to immune thrombocytopenic purpura associated with HIV infection, high dose IV IgG treatment (1-2 g/kg) also increases platelet counts but unlike other therapies for ITP, is not immunosuppressive and has no other serious adverse effects. It is likely that over the next few years, specific anti-HIV preparations will be evaluated. Neutralising antibody has been demonstrated in HIV-infected patients and a specific antibody preparation against HIV might either prevent HIV infection after initial exposure to the virus or slow the progression of HIV-related disease. However, the development of a specific, effective, neutralising anti-HIV immunoglobulin preparation (whether polyclonal or monoclonal) will require information about which HIV antigens elicit protective immunity and the role played by neutralising antibody in HIV-related disease.
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PMID:Immunoglobulin preparations for HIV-infected patients. 305 79

The Nucleic Acid Sequence-Based Amplification (NASBA) process involves alternate steps of DNA synthesis from an RNA template and RNA synthesis from a DNA template, using avian myeloblastosis virus (AMV) reverse transcriptase and T7 RNA polymerase, respectively. The overall fidelity of the amplification process was determined by sequence analysis of cloned DNA products of NASBA reactions. An error frequency of less than 0.3% was observed in cloned DNA products from two different segments of the HIV-1 gag gene. Partial substitution of GTP with ITP in the NASBA reaction did not significantly change the fidelity of the process. An error rate of 2 x 10(-4) was calculated for the combined effects of both polymerases.
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PMID:Fidelity of nucleic acid amplification with avian myeloblastosis virus reverse transcriptase and T7 RNA polymerase. 753 77

In summary, for intravenous gammaglobulin use of ITP in children and adults, it is clear that intravenous gammaglobulin is an effective way to increase the platelet count acutely and this will be faster than or as fast as any other therapy. However, there is no proven curative effect of IV gammaglobulin. Its use in situations requiring a rapid increase in the platelet count seems secure as does its use in children with chronic ITP. The latter however and the treatment of HIV-ITP may find IVIG treatment largely replaced in the future by IV Anti-D(10) which is currently experimental. The use of a viral inactivated form of IVIG currently seems mandatory to avoid post-transmission hepatitis.
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PMID:Uses of intravenous gammaglobulin in immune hematologic disease. 771 5

Recently there have been increasing reports of HIV infection acquired through transfusion of HIV seronegative blood in Thailand due to high incidence of HIV new infection in blood donors. Blood or blood components (BC) prepared from HIV seronegative blood donation pose significant hazards to recipients because of the risk of viremia during the "window period" of HIV infection. This paper presents the HIV seroprevalence in hematologic patients other than hemophiliacs who received multiple blood transfusion at Ramathibodi Hospital. The retrospective analysis was done on 167 patients: 132 thalassemia, 19 leukemia, 5 aplastic anemia, 5 ITP, 2 pure red cell aplasia, 2 congenital non spherocytic hemolytic anemia, 1 hereditary spherocytosis and 1 autoimmune hemolytic anemia patients, who received blood transfusion during January 1, 1987 till February 29, 1992 at the Department of Pediatrics, Ramathibodi Hospital. The number of blood or BC transfused in each patient was 1-154 units with the average of 23 units per patient per 5 years with a total 4,000 units. All were HIV sero-negative. Anti-HIV screening was performed periodically in these patients about 1-2 times per year or as necessary. The results were HIV seronegative in all cases. The reason for negative results cannot be explained clearly. It should be noted that our thalassemic patients receive leukocyte poor blood and avoid a hypertransfusion program. Patients with other blood diseases received both whole blood and BC. The HIV contaminated blood in the window period was estimated to be 1:10,000 in Thailand which showed HIV antigen positive but antibody negative. These patients may be fortunately received HIV non contaminated blood.
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PMID:HIV seroprevalence in hematologic patients other than hemophiliacs at Ramathibodi Hospital. 788 70

Human immunodeficiency virus 1-related idiopathic thrombocytopenic purpura (HIV-1-ITP) patients have a 4-fold increased percentage of CD5+ B cells and a 4.8-fold increased percentage of serum immune complexes precipitated by polyethylene glycol (PEG-ICs) compared to control subjects, as reported previously. Since CD5+ B cells produce predominantly IgM rheumatoid factor (RF) vs. Fc of IgG and PEG-ICs contain high levels of IgM, we looked for the presence of RF in the immune complexes of HIV-1-ITP patients. PEG-ICs were adsorbed to protein A and dissociated with acid, and IgM and IgG were purified by gel filtration and affinity chromatography. Solid-phase ELISA was used to measure antibody specificity vs. platelets, Fc, and HIV-1 gp120, p24, and CD4. Dissociated IgG antibody reacted with platelets, HIV-1 gp120, p24, and CD4, but not with Fc. Serum IgG did not react with platelets or Fc but did react with HIV-1 gp120, p24, and CD4. Both PEG-IC IgM and serum IgM reacted with Fc as well as the other four antigens. Control IgM and IgG were unreactive. Isolated IgM from PEG-ICs relocated approximately 50% of the IgG preincubated with IgM to the Vo region of a G200 gel-filtration column. Anti-platelet IgG but not IgM could be affinity-purified from fixed platelets. Both F(ab')2 fragments of anti-platelet IgG and the total PEG-IC bound to platelets in a saturation-dependent manner. F(ab')2 of anti-platelet IgG inhibited 50% binding of PEG-IC to platelets at an F(ab')2/complex ratio of 3:1 (wt/wt). Scatchard analysis revealed two classes of binding sites: high-affinity Kd values of 0.8-1.8 nM and lower-affinity Kd values of 6.6-12.3 nM with respective numbers of binding sites of 44,000-57,000 and 122,000-256,000 (n = 4). Anti-platelet IgG of 6/6 patients precipitated GPIIIa from platelet lysates of surface 125I-labeled platelets. Platelet count correlated inversely with anti-platelet IgG (r = -0.73; P < 0.01; n = 27). Thus, PEG-ICs of HIV-1-ITP patients contain IgM RF, which sequesters serum anti-platelet IgG containing anti-GPIIIa. Anti-platelet IgG contributes to binding of immune complexes to platelets and correlates with thrombocytopenia.
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PMID:Sequestration of anti-platelet GPIIIa antibody in rheumatoid factor immune complexes of human immunodeficiency virus 1 thrombocytopenic patients. 789 59

Selective tropism of human immunodeficiency virus (HIV) for cells with CD4 receptors and especially for TH lymphocytes--key cells in hematopoiesis--has from the clinico-biologic point of view a great many hematologic manifestations of which knowledge is essential for a good diagnosis and treatment as well as for a judicious estimation of prognosis. Thus the study presents the hematologic entities specifically associated with HIV infection (such as ITP, NHML) as well as the hematologic entities associated with HIV infection without presenting a causal relationship with the latter. The study also discusses the quantitative and morphologic changes of peripheral blood and of bone marrow often enlightening for the disease and its complications. An important chapter in the study is devoted to the hematologic changes induced by the HIV infection therapy as well as by the manners of therapeutic approach to the complex hematologic problems raised by the disease.
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PMID:Hematologic manifestations of infection with the human immunodeficiency virus. 792 Mar 33

13 patients with HIV-related immune thrombocytopenia (HIV-ITP) and 10 patients with chronic idiopathic thrombocytopenic purpura (C-ITP) were treated with a single course of alpha-2b-Interferon (IFN 3 x 10(6) IU subcutaneously for 12 d). The patients had platelet counts lower than 40 x 10(9)/L and thrombocytopenia persisting for over 1 year (range 1-22 years); 7 patients were refractory to previous conventional therapy, 5 were responsive, and 11 had not been previously treated. The response to IFN was complete in 8 patients (platelets > 100 x 10(9)/L), partial in 7 (platelets 50-100 x 10(9)/L); 8 patients showed no response. The treatment with IFN was stopped after 4 d in one patient due to a fall in platelet count. The maximal platelet count (median peak 116 +/- 55 SD x 10(9)/L platelets) was obtained after 13.7 +/- 2.98 d and the improvement in platelet count was maintained for 22.8 +/- 8.6 d. No difference in platelets response was observed between HIV-ITP and C-ITP. The response to IFN seems to be related to the one obtained with previous treatments. Indeed 80% of the patients who were responsive to previous steroids, high dose immunoglobulins or azidothymidine (HIV-ITP) showed a complete or partial response while only 43% of the refractory patients showed a partial response; the positive response rate in previously untreated patients was 73%.
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PMID:The effect of a single course of alpha-2B-interferon in patients with HIV-related and chronic idiopathic immune thrombocytopenia. 832 55

Patients with human immunodeficiency virus-type 1-immune thrombocytopenic purpura (HIV-1-ITP) have elevated polyethylene glycol (PEG)-precipitable immune complexes (ICs) composed of IgG, IgM, and complement that are threefold to sevenfold higher than in healthy control subjects. These complexes contain anti-F (ab')2 as well as anti-idiotype antibodies versus anti-HIV-1gp120. Because anti-F (ab')2 and anti-idiotype antibodies correlate with thrombocytopenia (r = .83 [J Clin Invest 77:1756, 1986] and r = .90 [J Clin Invest 89:356, 1992], respectively) we studied the binding of ICs to platelets and monocytes as well as their role in platelet-monocyte rosette formation. ICs bind to platelets in a saturation-dependent manner (optimum at 10 micrograms/mL; 0.5% of serum conc). Binding to platelets could not be inhibited with platelet saturating concentrations of aggregated IgG or with monoclonal antibody (MoAb) IV.3 versus FcR gamma II. Platelet binding could be inhibited with Fab anti-C3, anti-Clq, or anti-C4 by 57%, 40%, and 46% respectively, not with control Fab (P < .001). Monocytes from HIV-1-ITP patients form rosettes with normal platelets 16.8 +/- 5.2 rosettes/100 monocytes compared with 4.8 +/- 0.8 control monocytes plus normal platelets (P = .009). Gel-washed HIV-1-ITP platelets formed 19 +/- 2.0 rosettes with U937 cells compared to 6.3 +/- 1.0 for normal platelets (P = 0.001). Arming of U937 cells with HIV-1-ITP ICs (5 micrograms/mL) formed 36.7 +/- 2.5 rosettes compared with 10.6 +/- 1.2 for control ICs (P < .01). Rosetting of armed U937 cells could be inhibited with MoAbs versus the alpha chains of CD11a (LFA-1), 11b (Mac-1), or 11c (p150,95) by 67%, 70%, and 61%, respectively (P < .007), whereas binding of ICs to U937 cells was unaffected. Isotype-matched control as well as MoAbs versus antigens on U937 cells (CD13, CD33) or the anti-FcR gamma II receptor had no effect. However, Fab fragments of polyclonal anti-C3 inhibited rosette formation by 78% (P < .01); control Fab had no effect. Thus, platelet-monocyte rosette formation is not Fc dependent. It is complement receptor dependent and requires the cooperation of all three leuCAM integrins.
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PMID:Role of leuCAM integrins and complement in platelet-monocyte rosette formation induced by immune complexes of human immunodeficiency virus-type 1-immune thrombocytopenic purpura patients. 848 17

Our objective was to examine the efficacy and toxicity of continuous, low-dose interferon-alpha therapy for human immunodeficiency virus-related immune thrombocytopenic purpura (HIV-ITP) in a Phase II clinical trial overseen by a community-based consortium of physicians conducting clinical trials in HIV-related diseases. Sixteen patients with HIV-ITP defined by prospective clinical criteria were enrolled; the majority had failed other therapies for HIV-ITP. Baseline and serial measurements were made of platelet counts, complete blood counts, serum chemistries, platelet-associated immunoglobulin, and CD4+ T-lymphocyte counts; subjective symptoms and bleeding were recorded. Three million units of interferon-alpha 2b were self-administered by subcutaneous injection every Monday, Wednesday, and Friday for 16 weeks. Thirteen participants were evaluable for response. One obtained a complete response, eight had partial responses, and four had no response to interferon-alpha therapy. The mean absolute platelet count of the group rose from 15.5 x 10(9)/L at baseline to 47.3 x 10(9)/L at 2 weeks and remained in this range for the duration of the study. CD4+ T-lymphocyte counts and serum chemistries did not change significantly during therapy. Ability to detect platelet-associated immunoglobulin did not change in a predictable manner in relation to platelet count response. Hematologic toxicity was limited to one episode of granulocytopenia, which resolved after a lowering of zidovudine dosage. Subjective toxicities were mild and tolerable, and minor bleeding problems improved in all participants so affected. Low-dose, continuous therapy with interferon-alpha resulted in meaningful increases in the platelet counts of the majority of study participants with HIV-ITP. Interferon-alpha was safe and tolerable for most participants with HIV-ITP at the dosage and schedule employed in this study. Interferon-alpha for clinically significant thrombocytopenia and who have failed to respond to zidovudine.
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PMID:Continuous low-dose interferon-alpha therapy for HIV-related immune thrombocytopenic purpura. 854 45

Nondenaturing gel electrophoresis was used to study the nucleotide substrate-induced conformational change in reverse transcriptase (RT) of human immunodeficiency virus type 1 (HIV-1). Dead-end complex was formed between HIV-1 RT, dideoxynucleotide chain-terminated primer, and DNA template in the presence of deoxynucleotide triphosphate (dNTP) complementary to the next position on the template. Complexes which form in the absence of the next complementary dNTP were disrupted by adding excess poly(rA)/oligo(dT) or heparin just prior to electrophoresis. Dead-end complex formation by noncomplementary dNTP's or ribonucleotides was at least 2000-fold less efficient than with the complementary nucleotide. When dA was the next nucleotide on the template, analogues of dTTP supported dead-end complex formation with increased apparent Kd (dTTP < dideoxy-TTP approximately alpha-thio-dTTP < dUTP < 3'-azidothymidine triphosphate). A similar relationship was observed for dGTP analogues across from dC on the template (dGTP < dideoxy-GTP < alpha-thio-dGTP << dITP < dideoxy-ITP). The optimal length of the primer/template duplex region for dead-end complex formation was between 20 and 32 base pairs. Primer-template with a mismatched primer terminus did not support dead-end complex formation, and primer terminated with 3'-azidothymidine formed dead-end complex with 25-fold elevated apparent Kd. By contrast, dead-end complex formation on primer terminated with dideoxy-IMP base paired with dC on the template was more efficient than on primer terminated with dideoxy-GMP. Implications for the mechanisms of discrimination between nucleotide analogues by HIV-1 RT are discussed.
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PMID:Nucleotide-induced stable complex formation by HIV-1 reverse transcriptase. 915 15


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