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

Patients infected with the human immunodeficiency virus (HIV) may have an antibody deficiency and a deficiency of cellular immunity. Intravenous immunoglobulin (IVIG) preparations may benefit HIV-infected children and adults with recurrent bacterial infections at doses of 200 to 400 mg/kg every 2 to 4 weeks. In addition, IVIG (1 to 2 g/kg) is effective at raising platelet counts to hemostatic levels in HIV-infected patients with idiopathic thrombocytopenic purpura and life-threatening bleeding. Indirect evidence also suggests that IVIG may be effective in preventing Pneumocystis carinii pneumonia. Finally, recent studies suggest that specific anti-HIV antibody preparations may have a therapeutic role, either as immunoglobulin concentrates or as immunoadhesions and immunotoxins. However, further investigations are needed to exclude antibody enhancement of HIV infection by the Fc receptor or the complement receptor.
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PMID:Use of intravenous immunoglobulin in acquired immune deficiency syndrome. 187 43

Molecular fusions of CD4, the receptor for human immunodeficiency virus (HIV), with immunoglobulin (termed CD4 immunoadhesins) possess both the gp120-binding and HIV-blocking properties of recombinant soluble CD4, and certain properties of IgG, notably long plasma half-life and Fc receptor binding. Here we show that a CD4 immunoadhesin can mediate antibody-dependent cell-mediated cytotoxicity (ADCC) towards HIV-infected cells, although, unlike natural anti-gp120 antibodies, it does not allow ADCC towards uninfected CD4-expressing cells that have bound soluble gp120 to the CD4 on their surface. In addition, CD4 immunoadhesin, like natural IgG molecules, is efficiently transferred across the placenta of a primate. These observations have implications for the therapeutic application of CD4 immunoadhesins, particularly in the area of perinatal transmission of HIV infection.
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PMID:Biological properties of a CD4 immunoadhesin. 197 Jan 24

Evidence of antibody-dependent enhancement of human immunodeficiency virus type 1 (HIV-1) infection via Fc receptor (FcR) was published previously (A. Takeda, C. U. Tuazon, and F. A. Ennis, Science 242:580-583, 1988). To define the entry mechanism of HIV-1 complexed with anti-HIV-1 antibody, we attempted to determine the receptor molecules responsible for mediating enhancement of HIV-1 infection of monocytic cells. Monoclonal antibodies to FcRI for immunoglobulin G substantially blocked antibody-dependent enhancement of HIV-1 infection. Furthermore, we demonstrate a requirement for the CD4 molecule in antibody-enhanced HIV-1 infection via FcR. Soluble CD4 prevented infection by HIV-1 antibody-treated virus, and enhancement of infection of virus-antibody complexes was abrogated by a monoclonal antibody to CD4 (anti-Leu3a antibody). Treatment of human macrophages with an anti-CD4 antibody also inhibited antibody-enhanced HIV-1 infection of macrophages, supporting our contention that antibody-dependent enhancement of HIV-1 infection via FcR requires CD4 interaction with the virus glycoprotein.
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PMID:Two receptors are required for antibody-dependent enhancement of human immunodeficiency virus type 1 infection: CD4 and Fc gamma R. 197 24

Antibodies that augment human immunodeficiency virus (HIV) infectivity of monocytes through Fc receptor (FcR) type III for IgG have been found in the blood of sero-positive patients and immunized chimpanzees. This study investigated the effect of acute and chronic HIV infection, as well as protein kinase C activators capable of up-regulating latent HIV, on the expression of these receptors. In addition, the frequency of this antibody-dependent enhancement (ADE) phenomenon was estimated using purified IgG from HIV-1 seropositive individuals at various clinical stages of infection. The existence of an FcR-dependent pathway for ADE of HIV-1 infection in peripheral blood monocytes and promonocytic U937 cells was confirmed in sera from a small subset of patients, and the phenomenon extended to FcR types I and II. The level of ADE activity was minimal, however, and no relationship between the presence or magnitude of the ADE phenomenon and clinical stage was uncovered. Finally, perturbations which activate a latent HIV infection were shown to concomitantly up-regulate FcR on infected and uninfected cells. This suggests a positive feedback loop linking up-regulation of latent infection, enhanced expression of low affinity HIV receptors such as FcR, and viral spread.
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PMID:Human immunodeficiency virus infection of monocytes: relationship to Fc-gamma receptors and antibody-dependent viral enhancement. 214 69

The effect and mechanism of action of ImuVert, a new biological response modifier consisting of ribosomes and natural membrane vesicles of Serratia marcescens, on endogenous natural killer (NK) cells and activated NK activity has been analyzed. The studies showed that endogenous NK activity of peripheral blood mononuclear cells (PBMC) from normal cell donors was significantly increased (P less than 0.03) against K562, U937, and Molt-4 target cells. PBMC from cord blood of newborn infants lacking NK activity were upregulated (1.5-4 fold over endogenous NK activity) by ImuVert. Other studies showed that the abnormal NK activity of PBMC from patients with the human immunodeficiency virus (HIV) infection was significantly augmented in vitro (P less than 0.01) by ImuVert. ImuVert strongly stimulated interferon gamma production and in combination with interleukin 2 produced synergistically enhanced interferon gamma production and greater cytotoxicity than that induced by either alone. Studies on lymphocyte differentiation antigen expression following treatment with ImuVert indicated that ImuVert triggers interferon gamma production through binding the low affinity IgG Fc receptor, type III, CD16. The studies suggest that ImuVert may trigger interferon gamma production by binding to the Fc receptor and that the amplitude of the ensuing reaction and the ability of ImuVert to induce cytotoxicity in a setting where this activity has been down regulated is based on the absence of suppressor activation or direct contra suppressor activity.
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PMID:ImuVert activation of natural killer cytotoxicity and interferon gamma production via CD16 triggering. 214 37

Although CD4 is a major receptor for human immunodeficiency virus (HIV) infection of cells, studied by ourselves and others clearly show that the Fc receptor (FcR) also plays a role in infection, perhaps in conjunction with other surface receptors. IgG antibodies to HIV-1 will enhance infectivity in cells (such as monocyte-macrophages) that have surface Fc receptors; F(ab')2 fragments of antibodies did not enhance, and blocking of FcR inhibited enhancement. The high-affinity FcR for IgG (Fc gamma RI) appeared to be functional. Sera from HIV-1-infected patients had neutralizing activity at high concentrations, but enhanced infection at low concentrations (i.e., high dilutions). Our studies show that the CD4 receptor is required for antibody-mediated enhancement of infection, as enhancement can be blocked by recombinant soluble CD4 and by Leu3 antibody. Although enhancement can be demonstrated in vitro, the in vivo importance of enhancing antibodies remains to be defined in HIV-1 infection.
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PMID:FcR-mediated enhancement of HIV-1 infection by antibody. 222 46

Mononuclear phagocytes can be infected with the human immunodeficiency virus type 1 (HIV-1). Although these cells express CD4 antigen, which is the recognized cellular receptor for HIV, additional cell surface proteins such as the Fc receptor, might serve as receptors for infection. In order to study this possibility we used the U937 monocytic cell line as a target for HIV infection. Flow cytometry of U937 showed that 97% of cells expressed CD4, 33% expressed the high affinity 72 kD Fc receptor (FcRI), and 74% expressed the low-affinity 40 kD Fc receptor (FcRII). Virus neutralization tests were performed by preincubating heat-inactivated human anti-HIV sera with HIV-1, IIIB strain, and then challenging U937. After 13 days in culture, productive HIV-1 infection was monitored by reverse transcriptase activity. High concentrations of certain sera (10(-1)-10(-3) dilutions) neutralized HIV-1, but at subneutralizing concentrations (10(-4)-10(-6) dilutions), five of these sera enhanced viral infection approximately two- to threefold. This enhancement of HIV-1 infection was totally blocked by 1 microgram/ml recombinant soluble CD4 (rCD4) or by 0.5 microgram/ml anti-CD4 Leu3a monoclonal antibody. These results suggest that serum enhancement of HIV-1 infection, thought to be due to binding to the monocyte Fc receptor, requires HIV-1 binding to CD4, since rCD4 or Leu3a blocked this phenomenon.
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PMID:Inhibition of serum-enhanced HIV-1 infection of U937 monocytoid cells by recombinant soluble CD4 and anti-CD4 monoclonal antibody. 236 Oct 75

Antibody-dependent enhancement (ADE) of human immunodeficiency virus type 1 (HIV-1) infection in vitro has been described recently and was shown to occur by two mechanisms: either participation of the alternative pathway of complement or to involve an Fc receptor-mediated, complement-independent mechanism. Complement-mediated ADE results in an accelerated cytopathic effect in target cells that can abrogate the protective properties of neutralizing antibodies. This study characterizes the surface antigens of MT-2 cells using flow cytometric analysis and shows that these cells express high levels of both CD4 and complement receptor type 2 (CR2) while several CD4+ cell lines that do not demonstrate complement-mediated ADE lack high levels of complement receptors. Further, utilizing MT-2 cell cultures, it is demonstrated that complement-mediated ADE of HIV-1 infection is conferred by the sera from more than 80% of HIV-1 antibody-positive individuals (N = 85). Complement-mediated ADE of HIV-1 infection causes an acceleration of several parameters indicative of HIV-1 infection in vitro including increased HIV-1 antigen synthesis as detected by indirect immunofluorescence, RNA accumulation as measured by a solution hybridization protocol, reverse transcriptase release, and progeny virus production.
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PMID:Complement-mediated, antibody-dependent enhancement of HIV-1 infection in vitro is characterized by increased protein and RNA syntheses and infectious virus release. 246 4

Antibodies that enhance human immunodeficiency virus (HIV) infectivity have been found in the blood of infected individuals and in infected or immunized animals. These findings raise serious concern for the development of a safe vaccine against acquired immunodeficiency syndrome. To address the in vivo relevance and mechanism of this phenomenon, antibody-dependent enhancement of HIV infectivity in peripheral blood macrophages, lymphocytes, and human fibroblastoid cells was studied. Neither Leu3a, a monoclonal antibody directed against the CD4 receptor, nor soluble recombinant CD4 even at high concentrations prevented this enhancement. The addition of monoclonal antibody to the Fc receptor III (anti-FcRIII), but not of antibodies that react with FcRI or FcRII, inhibited HIV type 1 and HIV type 2 enhancement in peripheral blood macrophages. Although enhancement of HIV infection in CD4+ lymphocytes could not be blocked by anti-FcRIII, it was inhibited by the addition of human immunoglobulin G aggregates. The results indicate that the FcRIII receptor on human macrophages and possibly another Fc receptor on human CD4+ lymphocytes mediate antibody-dependent enhancement of HIV infectivity and that this phenomenon proceeds through a mechanism independent of the CD4 protein.
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PMID:The Fc and not CD4 receptor mediates antibody enhancement of HIV infection in human cells. 278 47

In studies aimed at defining monocyte and macrophage function in patients with human immunodeficiency virus (HIV) infection, we found impaired in vivo Fc receptor-specific clearance in 20 of 25 patients with acquired immunodeficiency syndrome (AIDS) and in five of 13 patients with AIDS-related illnesses. The in vivo function of macrophage C3 receptors was also found to be abnormal: AIDS patients had a relatively large release of cell back into the circulation, suggesting failure of macrophage phagocytosis. The antibody-dependent cell-mediated cytotoxicity of circulating mononuclear cells was significantly lower in AIDS patients than in healthy controls. Monocyte nonspecific phagocytosis and surface marker expression were intact. Defective monocyte and macrophage function is an integral part of the immunopathology of AIDS, leading to the failure to control opportunistic pathogens. Whether these defects are due to intrinsic infection of the mononuclear phagocytes with HIV or are secondary to other events in the network of HIV infection remains to be determined.
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PMID:Role of the mononuclear phagocyte system in the immunopathogenesis of human immunodeficiency virus infection and the acquired immunodeficiency syndrome. 270 32


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