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

Human Immunodeficiency Virus type 1 (HIV-1) infects CD4+ T lymphocytes and various other cell types, including B cells. Since HIV-1 seropositive individuals have high numbers of B cells carrying Epstein-Barr Virus (EBV), and are at high risk for development of EBV-associated lymphoproliferative diseases, we studied the mode of HIV-1 infection in four EBV-positive lymphoblastoid B-cell lines (LCLs) as well as some molecular and biological features of the B cells infected by both viruses. We found that LCL cells were successfully infected in vitro by HIV-1, despite the lack of CD4 antigen expression on the cell membrane. LCL cells displayed a persistent, productive, and non-cytopathic infection. Moreover, HIV-1 infection induced reactivation of EBV latent genomes in one cell line. Following HIV-1 infection, LCL cells showed a decrease in B-cell activation markers CD23 and CD39, and an increase in CD10 immature B-cell antigen. Not all cells in each LCL expressed HIV-1 antigens, but all CD10+ cells also co-expressed the HIV-1 envelope protein gp 120. Furthermore, HIV-1 infected LCL cells grew as disperse suspensions, and formed more agar colonies than control, non-HIV-1-infected LCLs. These findings raise the possibility that HIV-1 might play a role in EBV reactivation, and in B-cell lymphoma pathogenesis in AIDS patients.
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PMID:Morphological and phenotypical changes in EBV positive lymphoblastoid cells infected by HIV-1. 131 75

HIV-related non-hodgkin lymphomas currently occur in 5 to 8% of AIDS patients. AIDS-related lymphomas are high-grade tumors with the morphologic characteristics of either small noncleaved cell lymphomas of the Burkitt type or large cell centroblastic and immunoblastic lymphomas. Mixed features may be found, making classification difficult. Useful methods for characterizing AIDS-related non-hodgkin's lymphomas include immunophenotypic studies using B-cell differentiation and activation antigens (HLA-DR, CD10, CD19, CD20, CD21, CD22, CD23, CD38), evaluation of expression of surface immunoglobulins (IgS), activation and proliferation (CD25, CD30, CD71, Ki67), and identification of T-cell markers (CD1, CD2, CD3, CD4, CD5, CD7, CD8). Cases studied were of the B-cell type. Comparison with morphologic features revealed that Burkitt's lymphomas were monoclonal and expressed B-cell markers (CD10, CD19, CD20, CD22, CD38) and surface immunoglobulins, especially IgM kappa. This immunophenotype is similar to that of large cell or centroblastic non-hodgkin's lymphomas, suggesting that Burkitt lymphomas originate from centrofollicular cells. Immunoblastic non-hodgkin's lymphomas were monotypic or polytypic and expressed CD10 and CD38 antigens but not the other B-cell antigens Furthermore, a very large number of cells stained positively with the Ki67 antibody demonstrating that most lymphoma cells were undergoing cycling.
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PMID:[Non-Hodgkin's lymphoma and AIDS: histopathologic features]. 144 58

Trans-activating activities of certain cellular promoter/enhancer genes may reflect the underlying mechanism for cellular differentiation. We have used two promonocytic leukemia cell lines, U937 and HL-CZ, which differ in their differentiation antigen expression. While both cell lines express CD15 antigen, only the former expresses both CD4 and CD10 antigens. These phenotypes suggest that these two cell lines appear to be arrested at different stages of differentiation. Some regions of the long terminal repeat (LTR) of human immunodeficiency virus-1 (HIV-1) contain nucleotide sequences which bind cellular trans-activating factors such as NF-kappa B and Sp1. These sequences are also present in cellular regulatory gene sequences. The cell lines have been transfected by electroporation with a nested series of deletion mutants containing different lengths of the promoter/enhancer region for HIV-LTR. The promoter/enhancer region has been linked to a 'reporter' chloramphenicol acetyl transferase (CAT) gene. We have found that promoter/enhancer trans-activation is markedly enhanced by treating transfected cells with 12-O-tetradecanoylphorbol-13-acetate (TPA), while similar treatment with tumor necrosis factor-alpha (TNF alpha) slightly enhanced activation. U937 cells always showed much greater transactivating activities than did HL-CZ cells. Deletion of a negative regulatory element (NRE) from the LTR resulted in an enhanced transactivation, while deletions affecting NF-kappa B and/or Sp1 binding sites markedly reduced transactivation. Deletion of both NRE and NRF, a second negative regulatory factor binding site, from the LTR restored the transactivation. However, in the presence of TPA, deletion of NRE sequence without concomitant deletion of the downstream NRF binding sequence was sufficient for recovering transactivation. Since these two cell lines have shown subtle differences in these responses, it may be speculated that monocytes at different stages of differentiation may respond in different ways, qualitatively and/or quantitatively, to signal transduction factors involved in the transactivation of cellular genes.
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PMID:Regulation of cellular trans-activating activities in two different promonocytic leukemia cell lines. 191 29

Human cell lines (the T-cell lines H9, Jurkat, and HUT102, the myeloid lines U937 and HL60, and the Raji B cell line) were infected with HIV-1. HIV-1 antigen could be detected by immunofluorescence analysis in more than 50% of T cells and myeloid cells 15 days after infection. Infection of Raji cells took more than 2-3 months. Studies of cell surface marker expression revealed remarkable changes after HIV-1 infection of Raji cells: expression of CR2 (C3d/EBV receptor, CD19, CD20, CD22, CD23, CD10, and surface IgM) were highly reduced, in the case of CR2 and membrane-IgM from 100 to 0%, whereas levels of CD37 and CD38 remained unaltered by HIV-1 infection. U937 cells showed a reduction of CD4 expression from 14 to 5% after HIV-1 infection; the CR3 expression slightly increased from 25 to 30%. In contrast, HLA-DR was only expressed (21%) after HIV-1 infection but not in uninfected U937 cells. Expression of HLA-DR could be detected also in HL60 cells (33%) after HIV-1 infection. In H9 cells, CD4 was reduced from 60 to 30% after HIV-1 infection, whereas HLA-DR and CD25/IL-2 receptor expression increased from 16 to 90% and from 0 to 50%, respectively. CD4 was reduced from 70 to 0% from Jurkat cells after HIV-1 infection, whereas expression of CR2 was only slightly diminished from 8 to 4%. Expression of CR1 and HLA-DR was slightly increased in these cells (1 to 3%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of the C3d/EBV receptor and of other cell membrane surface markers is altered upon HIV-1 infection of myeloid, T, and B cells. 213 11

Four Epstein-Barr virus-positive lymphoblastoid cell lines (LCL) were successfully infected in vitro with immunodeficiency virus type 1 (HIV-1) as demonstrated by reverse transcriptase activity and p24 HIV antigen in culture supernatants, positive cell staining for gag-encoded HIV proteins, presence of viral HIV genome by Southern blot analysis and ulstrastructural observations. In addition, both HIV-1-infected B cells and their supernatants efficiently transactivated the chloramphenicol acetyl transferase reporter gene which is under the control of the HIV-1 long terminal repeat. The LCL cells displayed long-term HIV-1 infection and production, but no cytopathic effects were observed. Cytofluorimetric analysis did not detect membrane CD4 presence in the LCL cells before and after HIV-1 infection; moreover, a minute amount of CD4 mRNA was observed only in one of the LCL. A monoclonal antibody specific for the viral binding site of the CD4 molecule delayed, but did not block, HIV-1 infection of the LCL cells. Following HIV-1 infection, changes in LCL phenotype were observed, consisting of a decrease in CD23- and CD39-positive cells, and a concomitant increase of cells with surface CD10 and Bac-1. Furthermore, HIV-1-infected LCL cells did not grow in tight clumps, as usually observed in uninfected LCL, but as disperse suspensions, and formed more agar colonies than control LCL. However, despite this apparent acquisition of a malignant-like phenotype, c-myc proto-oncogene rearrangement was not detected. The appearance of cells with new characteristics did not seem due to clone selection by HIV-1 infection, since all the LCL conserved their clonotypic pattern of IgH chain rearrangement. The acquisition of malignant-like features by HIV-infected B cells might be clinically significant in terms of the pathogenesis of non-Hodgkin's B cell lymphomas, which occur frequently in AIDS patients.
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PMID:Infection of Epstein-Barr virus-transformed lymphoblastoid B cells by the human immunodeficiency virus: evidence for a persistent and productive infection leading to B cell phenotypic changes. 217 Jan 47

Plasma membrane-bound 5'-nucleotidase (5'-NT), gamma-glutamyltransferase (gamma-GT) and soluble deoxynucleotidyltransferase (TdT) were studied in peripheral blood cells (PBMN) of 35 individuals, 26 male and 9 female, with circulating anti-HIV antibodies. Twenty-six were drug abusers, 2 were drug abusers and homosexuals and 4 were homosexuals. Three did not fall into any risk group. The surface immunologic phenotype of cells stained with the fluorescent monoclonal antibodies Leu 5, Leu 3, Leu 2, Leu 12, Leu M3, Leu M1, anti-CALLA and anti-HLA-DR was delineated by flow cytometry. While the gamma-GT activity did not change, the lymphocyte 5'-NT activity was significantly less than normal in anti-HIV positive individuals and in anti-HIV negative drug abusers. TdT activity was detectable in 14 anti-HIV positive patients (40%), who did not have clinical AIDS. Of 8 patients with AIDS, 3 had a low level of TdT activity but 5 had cells completely devoid of TdT and 5'-NT activity. 5'-nucleotidase activity and the frequency of Leu 2 suppressor antigen bearing cells were the only independent variables that correlated with AIDS incidence.
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PMID:Enzymatic imbalance in peripheral blood mononuclear cells isolated from individuals with anti-HIV antibodies. 257 Jun 50

Using 14 well-defined (clustered) monoclonal antibodies (MAbs) against B-cell restricted/associated differentiation and activation (CD) antigens and 12 mediastinal clear-cell lymphomas (MCCL), 46 follicular-center-cell lymphomas (FCCL), and 20 non-neoplastic lymph nodes--including toxoplasmic and HIV-associated lymphadenitis--were immunohistochemically examined to determine the histogenesis of MCCL. Antigenically, MCCL was characterized as CD5-, CD10-, CD19+, CD20+, CD21-, CD22+, CD30-, CD37+, CDw40+, and by a frequent expression of CD11c and CD23, while other antigens were inconsistently expressed. The antigenic profiles of MCCL and FCCL showed statistically significant differences in 4/14 distinct antigens. When the neoplastic cells of both tumor groups were compared with morphologically defined normal B-cell types, the overall resemblance of their immunophenotypes was even closer between MCCL and sinusoidal (monocytoid) B cells than between FCCL and follicular-center B cells. We conclude that MCCL is a lymphoma type distinct from FCCL, most probably representing a highly malignant neoplasm corresponding to sinusoidal B-cell reaction.
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PMID:Immunophenotypic similarities of mediastinal clear-cell lymphoma and sinusoidal (monocytoid) B cells. 278 13

Peripheral blood mononuclear cells were quantified for the subsets of CD4, CD8, and CD19 lymphocytes by using CD45RA (2H4), CD29(4B4), CD57, CD5, CD10, Leu8, HLA-DR, and TCR gamma delta-1 monoclonal antibodies and dual color immunofluorescence. A comparative analysis of lymphocyte subpopulations was made among 52 HIV-infected and 50 age-matched control children and 30 HIV-seropositive and 27 negative control adults. A significant decrease in the CD4+CD45RA+ "naive" cells was much more marked in HIV-infected children than in HIV-infected adults. A significant percentage increase in the CD4+CD29+ "memory" cells was observed in HIV-infected children but not in infected adults; however, the absolute numbers were usually decreased in all age groups. The mean percentage and absolute numbers of CD4+CD7+ and CD4+Leu8+ cells were decreased in HIV-infected children, although usually not significantly. The CD3+TCR gamma delta-1+ did not show any change in the infected children tested. The mean percentage and absolute number of the CD8+HLA-DR+ cells increased significantly in HIV-infected persons of all ages. The CD8+CD57+ cells were increased in percentage and absolute number in HIV-infected children ages 1-4 and 4-8 years. In the adults, no change was noted in either the percentage or absolute number of CD19+CD5+ B cells, a finding similar to that noted in HIV-infected children above 1 year of age. Although adults showed a significant decrease in both percentage and numbers of CD5- B cells, an increase was noted in the 7- to 12-month-old HIV-infected children. The CD19+CD10+ cells showed a slight but significant decrease in the youngest age group and a significant increase in the older age groups of HIV-infected children. These findings indicate that several lymphocyte subpopulations are altered differentially during HIV infection in children of varying ages and in adults.
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PMID:Subpopulations of T and B cells in perinatally HIV-infected and noninfected age-matched children compared with those in adults. 751 Oct 82

Previous studies have shown that complement receptor 1 (CR1) expression on erythrocytes is decreased under several conditions including HIV infection and autoimmune diseases. The goal of this study was to determine whether expression of CR1 on peripheral blood B cells, where this receptor plays a role during immune responses, is altered in persons with HIV infection. The B cells from rheumatoid arthritis (RA) patients were also assessed since this represents a group with known complement and B cell abnormalities. The CD19+ B cells from persons with either HIV infection or RA had significantly reduced levels of CR1 when compared with control donors (75 and 72% CR1+ versus 94% CR1+ for control donors). The reduction of B cell CR1 occurred in both the percentage of B cells positive for CR1 and the levels of CR1 found on positive cells. In contrast, CR1 on monocytes was not reduced. As shown in previous studies, CR2 was also found to be reduced on B cells from the HIV-infected persons and there was extensive overlap between the B cell subsets which lacked expression of CR1 and CR2. The complement receptor-negative B cells found in HIV-infected persons were not immature or activated as defined by their lack of expression of CD10 or B7, respectively. Elevated levels of C4d, a classical complement pathway-activation product, were detected in plasma from both HIV-infected and RA patients. These studies suggest that chronic complement activation occurring in persons with HIV infection or RA can affect the complement receptor phenotype of peripheral blood B cells. Since complement receptors are involved in activation of B cells, the subset that lacks CR1 may represent cells that have encountered immune complexes and may therefore be stimulated. Additionally, the downregulation of complement receptors may have significant effects on the ability of B cells to capture and present opsonized antigens.
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PMID:Decreased levels of complement receptor 1 (CD35) on B lymphocytes in persons with HIV infection. 753 82

The anti-AIDS drug, [D-Ala1] Peptide T amide (D-ASTTTNYT.NH2) is an octapeptide which competitively inhibits the attachment of HIV to the receptor CD4 molecule on the T-lymphocyte. The objective of the study is to investigate the degradative process of this peptide and its effective enzyme inhibitors. The metabolites of [D-Ala1] Peptide T amide in rabbit brush-border membrane vesicles at pH 6.5 are ASTT, ASTTTN, YT and Y. The sequential time-course study of each metabolite reveals that enkephalinase (EC 3.4.24.11) plays an important role in the hydrolysis of [D-Ala1] Peptide T amide to ASTT. With the addition of an enkephalinase inhibitor, thiorphan, 85% of degradation was inhibited. Aminopeptidase is also involved in its degradative process and 25% of inhibition was observed by amastatin, an aminopeptidase inhibitor. The results show that no significant difference was observed between the in situ and chronical loop perfusion studies and enzyme activities are somewhat inhibited under acidic conditions in both methods. Approx. 90% of the parent peptide remained when rats were perfused with pH 4.0 peptide solution at a flow rate of 0.123 ml/min, while only 60% was recovered when pH 6.5 peptide solution was applied. The addition of amastatin made a quadrupled increase in the amount of parent peptide recovered. A 117-fold increment was observed when thiorphan was added. The dimensionless wall permeability of this peptide was 1.19 +/- 0.16 when pH 4.0 peptide solution was used during chronical loop perfusion study. Therefore, this study suggests that [D-Ala1] Peptide T amide could be absorbed via small intestine where enzymatic degradation s a rate-limiting step for the absorption of this peptide.
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PMID:Investigation into the intestinal metabolism of [D-Ala1] peptide T amide: implication for oral drug delivery. 765 67


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