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

Serum levels of soluble CD14 were elevated in HIV-infected asymptomatic patients or those with lymphadenopathy (CDC II/III) 2.9 +/- 0.8 mg/l compared with normal controls with 2.2 +/- 0.47 mg/l, P < 0.001. A further rise was seen in patients with ARC (CDC IVA) 3.8 +/- 1.1 mg/l, P < 0.01 and patients with AIDS (CDC IVB-D) 5.7 +/- 2.5 mg/l, P < 0.01. Although absolute numbers of CD14+ cells decrease in the AIDS group, the percentage of CD14+ monocytes did not change. In contrast, levels of soluble T cell antigens sCD4 and sCD8, which are higher in HIV-infected patients compared with normal subjects, showed no increase with disease progression. Serum levels of sCD14 were correlated positively with beta 2-microglobulin levels (rs = 0.63, P < 0.0001). Whereas the percentage of CD14+ monocytes did not change, an increase in monocytic CD14 expression in HIV-infected patients was observed (P < 0.01). The percentage of a monocyte subset expressing both CD14 and CD16 increased from 6% in normal healthy persons to 13% in HIV-infected patients (P < 0.001), and did not vary between the HIV patient groups. Incubation of cultured peripheral blood monocytes with azidothymidine had no effect on either normal or LPS-induced or IL-4-inhibited sCD14 release in vitro. Therefore, an effect of AZT on sCD14 serum values in vivo is considered to be unlikely. Our data further provide evidence that monocytes/macrophages are engaged in HIV infection.
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PMID:Increased soluble CD14 serum levels and altered CD14 expression of peripheral blood monocytes in HIV-infected patients. 752 38

Placental macrophages (Hofbauer cells) were isolated and cultured in vitro to investigate their susceptibility to human immunodeficiency virus type 1 (HIV-1) infection. Of adherent cells, 80% expressed CD14, and > 99% were nonspecific esterase-positive. CD4 antigen was expressed at very low levels. CD4 mRNA could be detected in the cells by reverse transcription followed by polymerase chain reaction. The macrophages were infected productively after inoculation with low-passage blood isolates of cell-free HIV-1. Peak virus titers were detected 3-7 days after infection by HIV-1 antigen ELISA and reverse transcriptase assay. Replication of HIV-1 in placental macrophages was less than in blood monocytes. HIV-1 RNA was detected in placental macrophages by in situ hybridization 16 days after infection. Multinucleated giant cells were identified in some cultures, indicative of an HIV-induced cytopathic effect. Thus, placental macrophages can be infected productively with clinical isolates of HIV-1, and such cells may act as a reservoir of virus for transmission to the fetus in utero.
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PMID:Human immunodeficiency virus type 1 infection of human placental macrophages in vitro. 768 88

In this study we evaluated the phenotype of alveolar mononuclear phagocytes recovered from the bronchoalveolar lavage fluid of 24 patients with human immunodeficiency virus infection (AIDS-related complex 8 patients. AIDS 16 patients) and 8 healthy individuals by using a panel of monoclonal antibodies known to react with tissue macrophages, in combination with a flow cytometer. The results showed that 90% of patients with AIDS present a marked reduction in the expression of several antigenic determinants (in decreasing order: CD68, CD36, CR1, CD11c, HLA-DR). The levels of antigen expression by flow cytometry seem to decline with disease progression, showing the most dramatic perturbations in patients with full-blown AIDS associated with pulmonary infections (especially Pneumocystis carinii pneumonia) and lower peripheral CD4 lymphocyte counts. In contrast, patients with AIDS-related complex or AIDS without histological or cultural evidence of pulmonary involvement showed, respectively, only minimal or medium antigenic decreases. However, only a minor proportion (16%, 20%, 20%, 25%, and 25% respectively) of human immunodeficiency virus infected patients (mostly with AIDS) had a significant reduction of the levels of CD4, CD14, CD45R, CD11b, and CD16 antigens in the alveolar macrophages. Since macrophages play a central role in the pathogenesis of AIDS, it may be postulated that the loss of various phenotypic markers on alveolar mononuclear phagocytes (some of them known for their important immunoregulatory actions) could have an important part in the pathogenesis of human immunodeficiency virus induced immunosuppression, and thereby condition the abnormal susceptibility to pulmonary diseases typical of human immunodeficiency virus-infected patients.
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PMID:Reduced expression of macrophage-associated antigens on alveolar mononuclear phagocytes from acquired immunodeficiency syndrome. 769 Dec 71

The "Centers for Disease Control" (CDC) recently published the guidelines for the performance of CD4+ T-cell determinations in persons with Human Immunodeficiency Virus (HIV) infection. Especially, a monoclonal antibody panel for lymphocyte immunophenotyping has been recommended i.e CD45/CD14, isotypic controls, CD3/CD4, CD3/CD8, CD3/CD19, CD3/CD56+ and/or CD16+. The authors compared, in 50 HIV+ patients, this method with the conventional method used in their laboratory i.e CD4/CD8 associated with isotypic controls. The mean values of CD4+ and CD8+ cells obtained using dual color immunophenotyping CD3/CD4 and CD3/CD8 did not differed significantly as compared with the values obtained using dual color immunophenotyping CD4/CD8. Especially, concerning CD4+ cells, differences did not exceed 4% considering each patient and 1% considering the mean values. However, in some patients, the differences between the levels of CD8+ cells obtained using the two methods were greater than 10%. These differences were due to an important percentage of CD3-CD8+ cells corresponding to NK cells. In another hand, there was no significant difference between the levels of CD4 and CD8+ cells obtained with or without correction using the gating reagent CD45/CD14. In conclusion, monoclonal antibody pannel recommended by CDC for lymphocyte immunophenotyping in HIV patients do not seem necessary in all cases. Analysis for CD4 and CD8 positive cells could be accomplish by three color simultaneous method (CD3/CD4/CD8), by first gating on CD3 positive T lymphocytes in order to eliminate both monocyte and NK cell contamination.
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PMID:[Evaluation of tests recommended by the CDC for the determination of CD4+ T lymphocytes in patients infected by the human immunodeficiency virus]. 775 91

Follicular dendritic cells (FDC) are restricted to the B-cell regions of secondary lymphoid tissue and to non-Hodgkin's lymphomas derived from the follicular center or the mantle zone. With their cytoplasmic ramifications they form a dense network which contains the B-lymphocytes. In situ, FDC are only detectable at the ultrastructural level or when stained with anti FDC-reagents. On the surface of their dendritic extensions they express transferrin receptors (CD71), the B-cell epitope CD20, class II antigens, the myelomonocytic molecule CD14, the glycoprotein gp50 (CD40), and several receptors for components of the complement system (CD11b, CD21, CD35). Subsequent to an antigen challenge, FDC trap and retain immune-complexes for a long period of time. In vitro FDC and neoplastic lymphocytes spontaneously form small cellular aggregates. This adhesion is mediated by the LFA-1-alpha/beta = ICAM-1, the VLA-4 = VCAM-1, and the ICAM-1 = C3bi- receptor ligand pathways on B-cells and on FDC, respectively. The loss of LFA-1- alpha/beta and ICAM-1 molecules may enable neoplastic lymphocytes to detach from FDC. The monoclonal B-cells now invade new compartments. In vitro, FDC have the capacity to activate resting B-cells and to save them from dying by apoptosis. Signals involved in this activation include cell-surface immunoglobulin and CD40. Immunocytochemistry and autoradiography with single cell suspensions of neoplastic B cells suggest that FDC also provide signals leading to the continued stimulation of lymphoma lymphocytes. During the early stage of HIV infection lymph nodes show an immense follicular hyperplasia, with a massive increase of the dendritic network of FDC. In the later stage of the disease, the continuous involution of the germinal centers is associated with a progressive destruction of FDC.
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PMID:Follicular dendritic cells in non-Hodgkin's lymphomas. 785 1

We determined the relative abilities of cell subpopulations from all major PBMC lineages of normal donors to produce IFN-alpha in response to in vitro stimulation with lymphocytotropic HIV-1 (IIIb and RF), monocytotropic HIV-1 (BaL), Sendai virus, and HSV-1. Active and inactive cell-free preparations of HIV-1 IIIb and cell-associated HIV-1 IIIb, and active cell-free preparations of the other viruses, induced comparable, maximal levels of acid-stable IFN-alpha in PBMC by 18 to 24 h. Negative selection and enrichment experiments indicated that HLA-DR+ "null" cells produced the majority of the IFN-alpha. A positive selection protocol using flow cytometric sorting enriched these HLA-DR+ CD3- CD19- CD16- CD56- CD14- cells to > 95% purity. These were identified as dendritic cells by their phenotype, large size, and veiled and ruffled morphology. The purified dendritic cells produced as much as 60-fold more IFN-alpha compared with purified, HLA-DR+ CD14+ monocytes in response to the viruses. IFN-alpha was not produced by CD3+ T cells or CD56+ NK cells. Purified CD19+ B cells produced a minimal amount of IFN-alpha in response to Sendai virus, and no IFN-alpha in response to the other viruses. Of significance, the dendritic cells expressed CD4 at a density similar to monocytes, and induction of IFN-alpha by HIV-1 could be blocked by HIV-1 gp120 anti-serum or anti-CD4 mAb. We conclude that the production of IFN-alpha constitutes a previously unrecognized major function of blood dendritic cells. This may be a mechanism of innate immunity mediated by dendritic cells against HIV-1 and other viral infections.
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PMID:CD4+ blood dendritic cells are potent producers of IFN-alpha in response to in vitro HIV-1 infection. 790 20

Placental macrophages were isolated and cultured in vitro to investigate their susceptibility to HIV infection and possible role in vertical transmission of HIV. After 10 days of in vitro culture the cells were positive for nonspecific esterase and acid phosphatase and negative for myeloperoxidase and placental alkaline phosphatase. They expressed cell surface HLA-ABC, HLA-DR, CD45, as well as CD68 intracellularly, as detected by flow cytometry, confirming their macrophage lineage. Approximately 80% of cells expressed surface CD14. CD4 antigen was expressed at very low levels and was confirmed by antibody blocking experiments. Infection of placental macrophage cultures with HIV resulted in a transient peak of viral replication 3 to 7 days after infection, but no later rise in HIV was detected with culture of up to 60 days. HIV replication was not up-regulated by coculture with phytohemagglutinin-stimulated lymphocytes or by treating infected cultures with tumor necrosis factor alpha or granulocyte-macrophage colony-stimulating factor.
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PMID:HIV infection of placental macrophages: their potential role in vertical transmission. 808 96

Blood monocytes as well as cells of the macrophage-phagocytic system in several tissues are targets for HIV-1 in vivo and in vitro. However, the data on HIV-1 infection of liver macrophages/Kupffer cells (KCs), which make up the main pool of fixed-tissue macrophages, is controversial. We therefore studied HIV-1 infection of KCs in vivo. Blood and liver tissue was obtained from seven AIDS patients shortly after death. Liver tissue was minced before processing. Cell suspensions were further purified by density gradient centrifugation, stained with anti-CD14 (blood monocytes) or anti-macrophage 25F9 (KCs), and separated by fluorescence-activated cell sorting (FACS). These highly purified cell populations were then analyzed for HIV-1 proviral DNA by the polymerase chain reaction (PCR). By performing PCR on FACS-purified cell populations, we could show that both KCs and peripheral blood monocytes were HIV-1-infected in 3 of 7 patients. KCs harbored HIV-1 proviral DNA only if peripheral blood monocytes were infected. These data show that KCs of the liver are infected with HIV-1 in vivo.
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PMID:Human Kupffer cells infected with HIV-1 in vivo. 809 11

We investigated the effect of human immunodeficiency virus type 1 (HIV-1) recombinant gp120 (rec.gp120) on phenotype and function of cultured monocytes. Rec.gp120 significantly reduced the accessory function of monocytes to stimulate autologous lymphocytes with anti-CD3, the Fc receptor-mediated chemiluminescence of monocytes, and the expression of CD4 and Fc receptor I/II, while the expression of the monocyte marker CD14 and major histocompatibility complex class I and II was not influenced. According to these phenotypic results, preincubation of monocytes with rec.gp120 depressed anti-CD3 antibody-induced T cell stimulation and Fc receptor-mediated phagocytosis as determined by chemiluminescence. Interferon-gamma release of lymphocytes induced by purified protein derivative of tuberculin was enhanced by gp120. These effects of isolated gp120 on monocyte immune functions in vitro might contribute to the understanding of the pathophysiology of HIV-1 infection in vivo.
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PMID:HIV-1 envelope protein gp120 affects phenotype and function of monocytes in vitro. 814 26

Human immunodeficiency virus type 1 (HIV-1) seropositive donors typically have high serum antibody titers to a range of autoantigens, and the corresponding autoantibodies have been suggested to be of importance in the pathogenesis of HIV-1 infection. We have prepared 38 IgG human monoclonal autoantibodies from asymptomatic HIV-1 seropositive donors with elevated serum titers to autoantigens by construction of Fab combinatorial libraries on the surface of phage and affinity selection using a range of autoantigens, including double-stranded DNA, major histocompatibility complex class II, CD14, epidermal growth factor receptor, and ganglioside GD2. The autoantibodies are shown to be of moderate affinity and exhibit marked cross-reactivity with a range of antigens. This contrasts with the specific high-affinity antibodies selected (i) against infectious agents using the same libraries and (ii) against one of the autoantigens using a library from a donor with established autoimmune disease. The results lend no support to the presence of specific autoantibodies in HIV-1 infection and instead suggest attention should be focused on the pathological significance of high serum levels of antibodies capable of interacting with multiple molecular species.
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PMID:The nature of the autoimmune antibody repertoire in human immunodeficiency virus type 1 infection. 817 Sep 74


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