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

Animal cells differ in susceptibility to HIV-1 infection. To identify rodent cells which are permissive to HIV-1 replication, we transfected murine and rat cells with an infectious clone of HIV-1 and a vector containing the chloramphenicol acetyl transferase gene under the control of HIV-1 LTR. Three groups of transfectants were distinguished: (i) Cells which permit neither HIV-1 LTR activation nor viral protein expression; (ii) Cells which permit activation of the HIV-1 LTR but not HIV-1 protein expression; and (iii) Cells which are fully permissive to both HIV-1 LTR activation and virus production. The latter included rat embryonal fibroblastoid (Rat2) cells, which, in short-term transfection assays, produced titers of HIV-1 proteins similar to transfected T lymphoid cells. To establish persistently infected cells, Rat2 cells were stably transfected with a plasmid containing an infectious clone of HIV-1/N1T-A and a neo gene, yielding several G-418-resistant, HIV-1-producing cell cultures. Of these, Rat2/A1 and Rat2/A2 cell cultures expressed up to 60 ng HIV-1 p24 core antigen per 1 x 10(6) cells 3 days after cell subculture over a period of 3 months. Southern blot hybridization revealed that Rat2/A1 and Rat2/A2 carried one to two HIV-1 DNA copies per cell; no rearrangements or deletions in viral DNA were present. Restriction endonuclease analysis of HIV-1 DNA in Rat2/A2 cells suggested clonal expansion of cells containing integrated HIV-1 genome. Virus produced by the Rat2/A1 cells was infectious in human T cells. These data demonstrate that some rodent cells have no inherent restriction to persistent and efficient production of infectious HIV-1.
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PMID:The establishment of rodent cell lines persistently producing HIV-1. 172 96

Germinal centers in lymph nodes with follicular hyperplasia from 15 patients with HIV-1 infection were analyzed by qualitative and quantitative electron microscopical methods and compared with control follicular hyperplasia (FH). Using a pattern recognition method, two main clusters were recognized within the germinal centers of HIV and FH lymph nodes on the basis of the relative frequencies of small centroblast and centrocytes. All FH lymph nodes and 6 HIV-1 lymph nodes (HIV-Clu-1) were placed in cluster 1; 9 HIV-1 lymph nodes (HIV-Clu-2) formed cluster 2. Germinal centers in the HIV-Clu-2 lymph nodes were characterized by a cell composition of predominantly lymphoid blasts and decreased numbers of centrocytes, but without altered numbers of mitotic figures. The frequency distribution of ultrastructurally distinct FDC subtypes differed between these clusters. In HIV-Clu-2 the frequencies of FDC types with an undifferentiated and regressive morphology occurred at a higher frequency, whereas FDC types with a highly differentiated morphology had a lower frequency. We conclude that 9 out of 15 lymph nodes with HIV-1 associated follicular hyperplasia show changes in FDC morphology indicative of a less differentiated functional stage of FDC. The changes in FDC morphology are closely associated with changes in the germinal center B-cell population resulting in an inverted blast to the centrocyte ratio.
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PMID:Cellular composition of germinal centers in lymph nodes after HIV-1 infection: evidence for an inadequate support of germinal center B lymphocytes by follicular dendritic cells. 173 Jan 53

Pathological abnormalities of the thymus were found in 3 of 37 fetuses aborted from human immunodeficiency virus (HIV)-infected mothers. These lesions were located predominantly in the thymic cortex, which contains mostly immature lymphocytes. Areas of focal lymphocyte depletion were infiltrated with CD4+ macrophages and were associated with abnormalities of the epithelial stromal network. No evidence of extensive HIV infection in any of the 37 thymuses was detected by either immunofluorescence or in situ hybridization techniques, although rare cells that expressed HIV antigens were found in 3 fetuses. Although less extensive, this thymic fetopathy was similar to that described in postnatal acquired immunodeficiency syndrome thymuses, strongly suggesting that the lesions were related to HIV infection. Thymic fetopathy might represent the initial injury to the lymphoid system in HIV-infected infants in whom early and severe immunosuppression develops.
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PMID:Thymic abnormalities in fetuses aborted from human immunodeficiency virus type 1 seropositive women. 173 99

The aim of this study was to determine whether mannosyl-specific lectins, especially Concanavalin A (ConA), may bridge HIV-1 env glycoproteins to cell membranes to increase virus binding to its targets, and to what extent this lectin-carbohydrate interaction can modify HIV-1 infectivity for monocytic compared with lymphoid cells. Monocytic U937 and lymphoid CEM cells, which both express surface mannose, were utilized. Whether first incubated with env glycoprotein or with the cells, lectins bound both to the cells and to radiolabeled recombinant gp160 (rgp160). Thus, they enhanced rgp160 adsorption to the cells in a methyl-alpha-mannose inhibitable manner. ConA did not appear to bind to the V1 domain of CD4 at the U937 cell surface since Leu3a binding was not blocked in the presence of ConA, nor was recombinant CD4 retained on a ConA-agarose affinity matrix. Moreover, enhanced rgp160 binding to the cells was CD4 independent, since it was not modified by preincubating the cells with Leu3a. Finally, ConA did not inhibit the binding of CD4-IgG3 chimeric molecules to virions immobilized on nitrocellulose membrane, which argues against the possibility that it interferes with the interaction of gp120 and CD4. However, both when incubated with the virus or with the cells and despite mediating enhanced binding of env glycoprotein, ConA neutralized HIV-1 infectivity for monocytic U937 as well as for lymphoid CEM cells. In this respect, ConA behaves like neutralizing antibodies which do not interfere with CD4 binding of gp120 but rather with some later event that leads to virus entry. These findings obtained with plant lectins may be of relevance in vivo, inasmuch as endogenous mannosyl-binding proteins, which are known to function as opsonins, have been reported to inhibit in vitro infection by HIV-1.
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PMID:Lectin-carbohydrate interactions and infectivity of human immunodeficiency virus type 1 (HIV-1). 173 38

Long-term bone marrow cultures (LTBMC) have been infected by two isolates of human immunodeficiency virus type 1 (HIV-1) (HIV-1 LAV and HIV-1 NDK) at multiplicities of infection ranging from 10(2) to 2.10(6) tissue culture infectious units (TCIU) per 10(6) bone marrow mononuclear cells (BMMNC). These infected cells are nonproducer cells and the viruses can be rescued by coculture with peripheral blood lymphocytes, cord blood lymphocytes, or BMMNC and not by the CEM cell line. HIV-1 clearly is not cytopathic for these cells. Following production and growth of erythroid burst-forming units (BFU-E) and erythroid colony-forming units (CFU-E) for at least 6 weeks after infection with HIV-1 NDK, colony assays displayed a 50% inhibition of BFU-E production during 3 weeks of LTBMC. This was followed by a stimulation phase. On the contrary, HIV-1 LAV induces a 150% stimulation of BFU-E production, followed by 50% inhibition. Production of CFU-E was inhibited by 80-100% with the two isolates of HIV-1 after four weeks of LTBMC. Stimulatory and inhibitory activities were recovered from supernatants of infected LTBMC and lymphoid CEM cell lines, suggesting that HIV-1 induces release of a humoral factor responsible for disruption of hemopoietic progenitor cell production in vitro and consequently for hematologic abnormalities in AIDS patients.
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PMID:Modulation of normal human erythropoietic progenitor cells in long-term liquid cultures after HIV-1 infection. 173 41

We describe clinical and postmortem findings in a 44-year-old man with pulmonary hypertension and infection with the human immunodeficiency virus (HIV-1). Plexogenic angiopathy and veno-occlusive lesions were present, in addition to a mild, patchy pulmonary interstitial lymphoid infiltrate. The clinical data for 14 previously reported cases of HIV-associated primary pulmonary hypertension are summarized. We speculate that these vascular changes may be due to damage from a specific immune response to HIV.
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PMID:Primary pulmonary hypertension and human immunodeficiency virus infection in a non-hemophiliac man. 174 Mar 4

Our studies originally demonstrated that the v-rel oncoprotein repressed gene expression in chicken lymphoid cells, while it activated transcription in rodent fibroblasts. Here we report that the c-rel protein can activate expression of genes linked to kappa B motifs when low levels of endogenous kappa B-binding activity are present. In contrast v-rel, and to a lesser extent c-rel, inhibit NF-kappa B-mediated activation of the human immunodeficiency virus long terminal repeat (HIV LTR) in phorbol ester-stimulated HeLa cells. Competition assays show that v-rel competitively inhibits both NF-kappa B and c-rel-mediated transcriptional activation. Analysis of mutant HIV LTR-chloramphenicol acetyltransferase (CAT) constructs in which all Sp1 or both NF-kappa B elements have been deleted shows that NF-kappa B motifs are required for rel-mediated effects on gene expression. Transforming v-rel mutants compete efficiently with phorbol ester-activated kappa B factors, whereas a transformation-defective mutant of v-rel is impaired in this activity. Taken together, these results strengthen the hypothesis that v-rel functions as a dominant interfering member of rel family proteins. These results also suggest that the ability of v- and c-rel to activate or repress gene expression in specific cells may result from their capacity to compete with endogenous rel family proteins whose expression and/or activity are cell-specific.
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PMID:Transcriptional activity of rel family proteins. 174 Nov 61

Human immunodeficiency virus infection is a leading cause of immunodeficiency in children. The epidemic in children parallels that in women since most infected women are in the child-bearing age groups. The risk of vertical transmission of HIV from an infected mother to her infant ranges from 13% to 39%. Diagnosis of infection in the infant is complicated by the passive transfer of antibody across the placenta, making the use of standard serologic tests to confirm infection difficult. In children less than 15 months of age, a positive p24 core antigen test, a positive viral culture or AIDS defining criteria with immune abnormalities are required for diagnosis. HIV infection in children is chronic and multisystem characterized by immunologic and clinical deterioration with a higher incidence of serious bacterial infections, neurologic disease, and lymphoid interstitial pneumonitis. The cornerstones of management include close medical follow-up, good nutrition, and prompt diagnosis and treatment of infections. Certain children will benefit from therapeutic modalities such as Pneumocystis carinii pneumonia prophylaxis and/or intravenous gamma globulin. The antiretroviral drugs have improved the quality of life and increased survival. Several newer antiviral agents are presently in clinical trials.
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PMID:Pediatric HIV infection. An update. 175 32

Bone marrow biopsies from eighty-five patients with different stages of HIV infection were reviewed. Biopsies were generally indicated to evaluate peripheral blood abnormalities, but suspicion of lymphoma and other specific pathologies was another important indication. The histopathological features are described and are often suggestive of HIV infection but non-specific. Hypercellularity (72.9%), dysmyelopoiesis (78.8%), plasma cell hyperplasia (97.7%), lymphoid infiltration (27%) and histiocytosis with or without granulomata (11.7%) were the most striking abnormalities. Other frequent features include: increased stainable iron deposits, venous stasis and serous atrophy (gelatinous transformation). Marrow hypoplasia is rather infrequent (28.2%) and usually a terminal event of AIDS. Bone marrow biopsies revealed opportunistic and neoplastic complications in seven cases, with demonstration of pathogens in four cases (Mycobacterium avium, Cryptoccocus neoformans, Toxoplasma gondii and Leishmania donovanii) and malignant lymphomas in three other cases (one Burkitt's lymphoma and two Hodgkin's disease). Bone marrow biopsy provides useful information for the diagnosis and prognosis of HIV infection and for the diagnosis of complications.
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PMID:[Bone marrow changes at several stages of HIV infection, studied on bone marrow biopsies in 85 patients]. 175 64

A wide spectrum of hepatic lesions has been reported in AIDS, but it is not known whether the changes are related to the presence of human immunodeficiency virus type 1 (HIV-1). Therefore, we examined liver sections from 15 consecutively autopsied patients with AIDS for the presence of HIV-1 antigens p24 (core) and gp41 (envelope) by the avidin-biotin-peroxidase complex method using monoclonal antibodies. The most common histologic abnormalities noted were steatosis, portal inflammation, Kupffer cell hyperplasia, and focal hepatocellular and bile duct damage. Intra-hepatic opportunistic organisms were detected in six of 15 (40%) cases, with Mycobacterium avium-intracellulare being the commonest (four cases). Immunoreactivity for HIV-1 antigens was demonstrated in 12 of 15 cases (80%), with staining limited to Kupffer cells and other mononuclear cells characterized by a lymphoid morphology. Approximately the same number and type of cells were stained with both monoclonal antibodies and did not bear any relation to the degree of histologic abnormalities nor to the presence of opportunistic infections. The data suggest that some pathologic changes in AIDS livers are more likely the result of an indirect effect mediated by infected resident and circulating mononuclear cells than a direct cytopathic effect of HIV-1.
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PMID:Immunohistochemical studies of human immunodeficiency virus-1 in liver tissues of patients with AIDS. 175 70


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