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

Following the unexpected finding of antibodies to GBM in a patient with Pneumocystis carinii pneumonia in the absence of kidney abnormalities, the presence of anti-GBM antibodies was analysed in 14 patients with pulmonary P. carinii infection who did not have clinical evidence of autoimmune glomerulonephritis. Patients were divided into three groups: HIV- with P. carinii pneumonia (n = 4), HIV+ with P. carinii pneumonia (n = 5) and HIV- carriers of P. carinii without pneumonia (n = 5). As control groups, HIV- patients with community-acquired non-P. carinii pneumonia (n = 6) and healthy individuals (n = 16) were included. Anti-GBM antibodies, studied with a quantitative enzyme immunoassay (EIA) for anti-alpha3 chain of collagen IV antibodies, were detected in three out of the four HIV-patients with P. carinii pneumonia, but not in any individuals of the other categories. These results suggest that P. carinii alveolar injury or the host response to the organism could affect the basal membrane Goodpasture antigen or a similar antigen, and induces anti-GBM antibody production in HIV- patients, and support the hypothesis that, at least in some cases, Goodpasture's syndrome could be triggered by an alveolar lesion induced by a P. carinii pneumonia.
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PMID:Presence of glomerular basement membrane (GBM) antibodies in HIV- patients with Pneumocystis carinii pneumonia. 906 15

Xanthomas may be associated with benign or malignant lymphoproliferative diseases, often with associated hypergammaglobulinema. In human immunodeficiency virus type 1 (HIV-1) disease, there is a high lymphoproliferative rate despite the immunodeficiency and increased cell death. We report three HIV-1-positive patients with facial papular xanthomatosis eruptions associated with hypergammaglobulinema, and an immunoglobulin A (IgA) gammopathy. Histopathologic features include lipid-laden macrophages, extracellular nuclear dust with phagocytosized nuclear debris, and hyalinization with areas of hyaline necrosis of collagen fibers. These distinctive papular xanthomas may be a marker of HIV-1 disease and of a pattern of immunodysregulation, immunodeficiency, and lymphoid proliferation seen in HIV-1 disease.
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PMID:Histologically distinctive papular neutrophilic xanthomas in HIV-1 + patients. 915 78

Lobular hepatic fibrosis and the presence of myofibroblasts were studied in heroin abusers, by quantitative automatic image analysis. Nineteen addicts (DA) and thirteen patients having stopped consumption (exDA) were compared to a non-addict group (CONTROL). Addicts, all anti-HIV and HBsAg negative, showed increased transaminase levels. Hepatitis C markers were ot available, at the time of biopsy. The surface of the centrolobular fibrosis, measured on picrosirius stained slides, was respectively 1.9 and 3.5 times larger in DA and exDA than in CONTROL (p < 0.0001). Immunolabelling with an alpha-smooth muscle actin antibody (alpha-SMA) revealed stellate cells in a perisinusoidal location, mainly in areas of matrix thickening in the space of Disse. Morphometric analysis of alpha-SMA expression showed significant differences between the three groups of patients, p < 0.0001 (CONTROL: 198.06 +/- 5.59 microns2; DA: 2227.91 +/- 88.02 microns2; exDA: 3469.10 +/- 154.98 microns2). The surface density of collagen and of alpha-SMA reactivity was also significantly different between these groups (p < 0.0001). These data strongly suggest that heroin is responsible for an early and progressive centrolobular liver fibrosis, occurring simultaneously with a myofibroblastic response. It might represent a reparative phenomenon arising from a direct vascular injury, leading to an impairment of blood-hepatocyte exchange.
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PMID:Quantitative studies on liver fibrosis and alpha-smooth muscle actin expression in heroin abusers. 922 Jan 52

The pathogenesis of HIV infection involves a complex interplay between both the infected and noninfected cells of human lymphoid tissue, the release of free viral particles, the de novo infection of cells, and the recirculatory trafficking of peripheral blood lymphocytes. To develop an in vitro model for studying these various aspects of HIV pathogenesis we have utilized blocks of surgically excised human tonsils and a rotating wall vessel (RWV) cell culture system. Here we show that (1) fragments of the surgically excised human lymphoid tissue remain viable and retain their gross cytoarchitecture for at least 3 weeks when cultured in the RWV system; (2) such lymphoid tissue gradually shows a loss of both T and B cells to the surrounding growth medium; however, this cellular migration is reversible as demonstrated by repopulation of the tissue by labeled cells from the growth medium; (3) this cellular migration may be partially or completely inhibited by embedding the blocks of lymphoid tissue in either a collagen or agarose gel matrix; these embedded tissue blocks retain most of the basic elements of a normal lymphoid cytoarchitecture; and (4) both embedded and nonembedded RWV-cultured blocks of human lymphoid tissue are capable of productive infection by HIV-1 of at least three various strains of different tropism and phenotype, as shown by an increase in both p24 antigen levels and free virus in the culture medium, and by the demonstration of HIV-1 RNA-positive cells inside the tissue identified by in situ hybridization. It is therefore reasonable to suggest that gel-embedded and nonembedded blocks of human lymphoid tissue, cocultured with a suspension of tonsillar lymphocytes in an RWV culture system, constitute a useful model for simulating normal lymphocyte recirculatory traffic and provide a new tool for testing the various aspects of HIV pathogenesis.
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PMID:Lymphocyte trafficking and HIV infection of human lymphoid tissue in a rotating wall vessel bioreactor. 935 61

HIV-induced syncytia of the CD4+ SUP-T1 T cell line mimic the subcellular organization of single cells and are able to crawl like single cells through extension of giant pseudopods. Because syncytia have been demonstrated in lymphoid tissue of HIV-positive individuals, their behavior has been investigated on more natural substrata, including dehydrated collagen, hydrated collagen, endothelial monolayers, and endothelial monolayers grown on collagen cushions. On hydrated collagen gels, both individual SUPT1 cells and syncytia form unusually long cylindrical projections that possess pseudopodial ends and are highly dynamic. Syncytia penetrate collagen gels through extension of these projections and disrupt their integrity. When incubated on endothelium, both single cells and syncytia readily traverse the monolayer through holes, and when incubated on endothelium supported by a collagen cushion, syncytia generate large holes through the monolayer, penetrate the monolayer, and disrupt the collagen gel through extension of long, complex projections. Invading syncytia also release viruses in a polarized fashion which adhere to and are taken up in vesicles by the endothelium. It is suggested that the destructive behaviors of syncytia which have been demonstrated in vitro may have correlates in vivo.
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PMID:The invasive and destructive behavior of HIV-induced T cell syncytia on collagen and endothelium. 946 82

Freshly isolated human monocytes do not express p125(FAK) but upon adherence to substrata activate the highly related calcium-dependent tyrosine kinase (CADTK), also known as Pyk2, CAKbeta, RAFTK, and FAK2. The monocyte CADTK was 5 kDa smaller than protein from epithelial cells; isolation and sequencing of the monocyte CADTK cDNA revealed a predicted 42-amino acid deletion between the two proline-rich domains of the enzyme. The nucleic acid sequence suggests that the deletion is caused by alternative RNA splicing. This species was also found in T and B lymphocytes and appears to be the predominant form of cytoskeletal associated tyrosine kinase in non-neoplastic, circulating, hematopoietic cells. CADTK was not activated when monocytes maintained in suspension were treated with agents that produce an intracellular calcium (thapsigargin) or protein kinase C (phorbol 12-myristate 13-acetate) signal including a chemokine, RANTES, that binds to the HIV co-receptor, CCK5. In contrast, monocyte adherence to tissue culture plastic-stimulated CADTK tyrosine phosphorylation, a process that was enhanced by thapsigargin, phorbol 12-myristate 13-acetate, and RANTES but that was completely blocked by preincubation with cytochalasin D. When compared with plastic, adherence to fibronectin- or collagen-coated surfaces produced only minimal CADTK activation but permitted significant stimulation by added thapsigargin. These data suggest that in a cell type that lacks p125(FAK), CADTK plays an early role in post-adherence signaling. Its activation involves two stages, cytoskeletal engagement, which is permissive, and co-stimulatory signals (calcium or protein kinase C) generated by extensive cell surface engagement, agonists, or inflammatory chemokines.
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PMID:A calcium-dependent tyrosine kinase splice variant in human monocytes. Activation by a two-stage process involving adherence and a subsequent intracellular signal. 954 57

A case of malignant melanoma arising in a young patient suffering from human immunodeficiency virus (HIV) infection is reported, along with a review of the literature. The neoplasm was characterized by aggressive clinical behaviour and, histopathologically, by a peculiar retiform pattern of growth with neoplastic cells interspersed among collagen bundles in the dermis without evident fibroplastic stromal reaction. In addition, a complete absence of host inflammatory cell infiltrate was noted. We hypothesize that this unusual histopathological pattern of growth, which has never been reported in this clinical setting, might be associated to HIV disease, immunosuppression and poor clinical outcome.
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PMID:Malignant melanoma associated with human immunodeficiency virus infection: a case report and review of the literature. 961 Aug 75

The ability of blood coagulation factor XIII (FXIII) to affect collagen synthesis and degradation led to its use in the treatment of scleroderma. Encouraging initial results were achieved principally in terms of skin sclerosis, musculoskeletal involvement and weakness. Further assessment of this treatment in scleroderma was abandoned when, following the HIV epidemic, FXIII use became strictly regulated. Safer concentrates are now available which may allow us to reconsider this therapy. This paper, which briefly reviews available data related to FXIII use in scleroderma and which proposes general rules for prescribing, is aimed at generating an open debate as to the need to widen the regulated use of FXIII to scleroderma.
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PMID:Coagulation factor XIII in scleroderma. 964 77

Human immunodeficiency virus (HIV)-1 can invade the brain and cause degeneration of the central nervous system, resulting in a host of cognitive and motor impairments. HIV-1 glycoprotein 120 (gp120), has been implicated in the neurodegenerative effects of HIV infection. Here, gp120's neurotoxic potential is demonstrated in both transgenic mice and cultured cells. We observed that gp120 causes an induction of matrix metalloproteinase (MMP)-2 activity and protein in transgenic mouse brains and in transfected C6 cells. We propose that induced MMP-2 may contribute to a neurodegenerative environment by degrading extracellular matrix (ECM) fibronectin and type IV collagen.
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PMID:Induction of matrix metalloproteinase-2 in human immunodeficiency virus-1 glycoprotein 120 transgenic mouse brains. 977 29

We studied the prevalence of the hepatitis C virus (HCV), human immunodeficiency virus (HIV) and GB virus C or hepatitis G virus (GBV-C/HGV), and characteristics of infections in Japanese haemophilia patients. Haemophilia patients were highly infected with HCV (88.2%) because of frequent use of unheated blood concentrates. Analysis for HCV genotypes revealed characteristics of HCV infection in haemophilia patients. Japanese haemophilia patients were highly infected with rare genotypes in Japan: genotype 1a (26.5%), genotype 3 (14.5%) and genotype 4 (2.4%). HIV infection was observed in 32.3% of haemophilia patients. HCV quasispecies (clones) and direct sequencing were investigated in patients with a single HCV genotype in the hypervariable region 1 of HCV, which resulted in a high degree of diversity. This indicates that even a single genotype of HCV might have multiple origins. GBV-C/HGV infection was noted in 20.9% of Japanese haemophilia patients. Over 40 haemophilia patients with chronic hepatitis C have been treated with interferon alpha for 6 months at total doses of 480-720 million units. About 38% showed clearance of HCV RNA from serum. Six patients with HIV infection were included in the study and they did not show eradication of HCV from the serum. This might derive from that they had high serum HCV RNA titers and genotype 1a or 1b. Histologic assessment was performed in 36 haemophilia patients with HCV. No case showed a histologically normal liver. Hepatic fibrosis in the biopsy specimens was classified into five stages of fibrosis and compared with serum hepatic fibrosis markers. Serum hyaluronic acid mostly correlated with hepatic fibrosis (r = 0.78, P < 0.0001) followed by type IV collagen (r = 0.38, P < 0.05). This suggests that estimation of serum fibrosis markers might be substituted for liver biopsy in haemophilia patients.
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PMID:Assessment and treatment of liver disease in Japanese haemophilia patients. 987


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