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

Allogenic transplants have an established place in reconstructive procedures. For years it has been suspected that lyophilized dura mater can transmit Creutzfeld-Jakob disease. HIV infection with fully manifest AIDS and a mortality of up to 100% is now also increasing in significance. It is necessary to assess the risk of transferring HIV with allogenic transplants because HIV passes into the cell via specific surface receptors and is integrated within the chromosome. Experimental data on disinfection and sterilization of allogenic transplants stored within chromosomes and their inactivation are not available. Allogenic transplants are only used in operations for life-threatening disease. As a rule, these are elective operations which must meet the highest safety standards, also with regard to the danger of infection. Collaboration with a transplantation team is essential.
HNO 1991 May
PMID:[Risks of a cartilage-bone bank with reference to HIV infection]. 187 34

We report our experience with 209 HIV-positive patients in different stages. A retrospective study (n = 181) showed the high frequency of lymphadenopathy, inflammatory diseases of mouth, pharynx, and esophagus (especially candidiasis) as well as other diseases such as sinusitis. A retrospective study by radiology (n = 28) showed inflammatory changes in the paranasal sinuses in patients with LAS, ARC, and AIDS.
HNO 1988 Dec
PMID:[Sinusitis and other typical ENT diseases within the scope of acquired immunologic deficiency syndrome (AIDS)]. 323 61

AIDS dementia complex (ADC) is a complex, progressive neuropsychiatric syndrome seen in 60-70% of the patients with AIDS. The structural and functional changes associated with ADC may be the result of a variety of indirect mechanisms mediated via activated brain cells or/and virus that produce neurotoxins including N-methyl-D-aspartate receptor agonist (eg, quinolinic acid, glutamate), cytokines, gp 120 and nitric oxide. The level of the neurotoxin and kynurenine pathway metabolite, quinolinic acid, is increased in the brain and CSF of HIV-1-infected patients, and is correlated with quantitative measures of neurologic impairment. Importantly, increased CSF and brain levels of QUIN also occur in other inflammatory neurologic diseases (bacterial, viral, fungal and parasitic infections, meningitis, autoimmune diseases and septicemia), independent of HIV-1 infection. Therefore, QUIN and other neuroactive kynurenine pathway metabolites may be final common mediators of neurologic dysfunction in a broad spectrum of inflammatory neurologic diseases. Conversion of L-tryptophan to QUIN has also been demonstrated in vitro in both brain tissue following macrophage infiltration, and in macrophages stimulated by interferon-gamma or HIV infection. Macrophages in vitro have a high capacity to synthesize QUIN following exposure to interferon-gamma, tumor necrosis factor-alpha, IL-1 beta and IL-6, compared to cells derived from other tissues. Notably, the concentrations achieved in the macrophage incubates exceeded the levels found in the CNS of HIV-1-infected patients, and exceeded the concentrations shown to be neurotoxic in vitro. We hypothesize that increased kynurenine pathway metabolism following inflammation reflects the presence of macrophages and other reactive cell populations at the site of brain infection. Strategies to attenuate the neurotoxic effects of kynurenines, such as inhibitors of kynurenine pathway metabolism and cytokine antibodies may offer new approaches to therapy.
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PMID:[Biochemical studies on AIDS dementia complex--possible contribution of quinolinic acid during brain damage]. 747 52

Since early growth response-1 (Egr-1) is required for macrophage differentiation and nitric oxide (NO) is immunosuppressive, we hypothesized that NO would reduce Egr-1 expression in rat lung macrophages. The inflammatory stimuli interferon-gamma and lipopolysaccharide induced an early, transient increase in Egr-1 mRNA (> 5-fold at 2 h) and a sustained, high level of inducible NO synthase mRNA (> 100-fold from 4 to 24 h). The NO metabolites nitrite and nitrate rose > 10-fold in medium from stimulated versus unstimulated cells over 24 h. Concomitant with elevated nitrogen oxides, Egr-1 mRNA levels declined to 80% below unstimulated cells at 24 h. This decline was blocked by an inhibitor of NO production, NG-monomethyl-L-arginine. Further, the NO donor S-nitroso-N-acetylpenicillamine inhibited Egr-1 expression in a dose-dependent manner, producing complete inhibition at 0.5 mM. The effect of S-nitroso-N-acetylpenicillamine was not due to reduced macrophage viability. We conclude that Egr-1 induction precedes inducible NO synthase induction in stimulated rat macrophages and that subsequent NO production reduces macrophage expression of Egr-1. We propose that this mechanism is used to regulate macrophage differentiation in human immunodeficiency virus infection and other inflammatory states.
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PMID:Nitric oxide reduces early growth response-1 gene expression in rat lung macrophages treated with interferon-gamma and lipopolysaccharide. 752 82

Although microglia are the only cells found to be productively infected in the central nervous system of acquired immunodeficiency disease syndrome (AIDS) patients, there is extensive white and gray matter disease nonetheless. This neuropathogenesis is believed to be due to indirect mechanisms other than infection with human immunodeficiency virus 1 (HIV-1). Cytokines and toxic small molecules have been implicated in the clinical and histopathological findings in CNS AIDS. Previously, we have demonstrated in rodent glial cultures the presence of biologically active epitopes of gp120 and gp41 that are capable of inducing interleukin 1 and tumor necrosis factor alpha. In this study, we map the HIV-1 envelope epitopes that induce nitric oxide, inducible nitric oxide synthase, interleukin 1, and tumor necrosis factor alpha in human glial cultures. Epitopes in the carboxy terminus of gp120 and the amino terminus of gp41 induce these proinflammatory entities. In addition, we compare HIV-1 infection and pathology in glial cells derived from human brain taken at different states of maturation (fetal, neonatal, and adult brain) in an effort to address some of the clinical and histological differences seen in vivo. This study demonstrates that, in the absence of virus infection and even in the absence of distinct viral tropism, human glia respond like rodent glia to non-CD4-binding epitopes of gp120/gp41 with cytokine and nitric oxide production. Differences among fetal, neonatal, and adult glial cells' infectivity and cytokine production indicate that, in addition to functional differences of glia at different stages of development, cofactors in vitro and in vivo may also be critical in facilitating the biological responses of these cells to HIV-1.
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PMID:Human immunodeficiency virus 1 envelope proteins induce interleukin 1, tumor necrosis factor alpha, and nitric oxide in glial cultures derived from fetal, neonatal, and adult human brain. 756 97

To get a measure of the extent of induction of nitric oxide synthase in infection with human immunodeficiency virus type-1 (HIV-1) in vivo, we estimated serum nitrite plus nitrate concentrations in 110 HIV-1 infected individuals compared to 76 blood donors. To monitor cytokine action and to measure induction of pteridine synthesis, we determined in parallel neopterin, biopterin, soluble tumor necrosis factor-alpha receptor 55 and 75, and beta 2-microglobulin. Serum nitrite plus nitrate concentrations were elevated in patients as compared to blood donor controls. In sera of patients, nitrite plus nitrate levels correlated significantly with neopterin, soluble tumor necrosis factor receptor 55 and 75, and beta 2-microglobulin. Nitrite plus nitrate levels were higher and correlations were stronger in groups of patients with lower CD4+ cell count. These results suggest that cytokine-mediated nitric oxide synthesis occurs in individuals with HIV-1 infection.
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PMID:Serum nitrite plus nitrate in infection with human immunodeficiency virus type-1. 759 Aug 63

HIV-1 infection is characterized by multiple neurological syndromes occurring at all stages of infection. HIV-1-associated dementia, however, is the most devastating CNS consequence of AIDS because of its poor prognosis and functional impairment. A clinical triad of progressive cognitive decline, motor dysfunction, and behavioural abnormalities typifies this subcortical dementia which eventually affects 15 to 20% of AIDS patients. Neuroimaging, CSF studies and neuropsychological testing are frequently required in diagnosing HIV-associated dementia, to exclude other conditions including psychiatric illnesses, opportunistic diseases and systemic disorders. The pathogenesis of HIV dementia is uncertain and there is evidence that multiple mechanisms of neurological injury occur. These mechanisms include: the role of neurovirulent strains of HIV; the potential neurotoxicity of HIV gp120, nitric oxide and quinolinic acid; immunologically mediated CNS injury through the action of cytokines and arachidonic acid metabolites; and altered blood-brain barrier permeability. A collective approach involving clinical studies, in vitro assays and animal models will provide greater insight into the pathogenesis and the rational development of therapy for HIV dementia.
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PMID:HIV-1 associated dementia: clinical features and pathogenesis. 762 22

Abuse of nitrite inhalants is common among male homosexuals and a history of abuse has been correlated with seropositivity to HIV and with the incidence of Kaposi's sarcoma among AIDS patients. The present study shows that inhalation exposure of mice to 900 ppm isobutyl nitrite for 45 min/day for 14 days compromised macrophage tumoricidal activity by up to 40% and it remained compromised for at least 7 days after terminating exposures. The inhalation exposures did not affect tumor cell binding but did inhibit inducible nitric oxide (NO zero). The NO zero synthase inhibitor NG-methyl-L-arginine totally inhibited both NO zero production and cytotoxicity, suggesting that reductions in NO zero due to inhalant exposure may be responsible for the reduced cytotoxic activity. Exposure to the inhalant increased constitutive production of tumor necrosis factor-alpha (TNF-alpha). TNF-alpha has been reported to stimulate the replication of HIV and the proliferation of Kaposi's sarcoma cells in vitro.
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PMID:Inhalation exposure to isobutyl nitrite inhibits macrophage tumoricidal activity and modulates inducible nitric oxide. 782 66

Primary pulmonary hypertension (PPH) is at present little understood. It is characterized by extensive remodeling of the pulmonary vasculature, with consequent deleterious hypertrophic changes in the right ventricle. Median survival is 2.6 years, although this varies with the severity of right heart failure. Although PPH can occur at any age and in either sex, it primarily affects young to middle-aged women. A genetic predisposition appears to be a component of this disease, triggered by presentation of a stimulus (e.g., drugs or HIV infection). Symptomatic presentation includes exertional dyspnea, chest pain, and syncope. At present, therapy consists principally of anticoagulation, calcium antagonists, nitric oxide inhalation, or continuous intravenous prostacyclin.
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PMID:Pathology and pathophysiology of primary pulmonary hypertension. 784 55

This review aims to summarize recent work related to the pathogenesis and possible treatment of neuronal injury in the acquired immunodeficiency syndrome (AIDS), especially with reference to potential neurotoxic substances released by HIV-infected or gp120-stimulated macrophages/microglia. Approximately a third of adults and half of children with AIDS eventually suffer from neurological manifestations, including dysfunction of cognition, movement, and sensation. Among the various pathologies reported in brains of patients with AIDS is neuronal injury and loss. A paradox arises, however, because neurons themselves are for all intents and purposes not infected by human immunodeficiency virus type 1 (HIV-1). This paper reviews recent evidence suggesting that at least part of the neuronal injury observed in the brains of AIDS patients is related to excessive influx of Ca2+ after the release of potentially noxious substances from HIV-infected or gp120-stimulated macrophages/microglia. There is growing support for the existence of HIV- or immune-related toxins that lead indirectly to the injury or demise of neurons via a potentially complex web of interactions between macrophages (or microglia), astrocytes, and neurons. HIV-infected monocytoid cells (macrophages, microglia or monocytes), especially after interacting with astrocytes, secrete substances that potentially contribute to neurotoxicity. Not all of these substances are yet known, but they may include eicosanoids, i.e. arachidonic acid and its metabolites, as well as platelet-activating factor. Other candidate toxins include nitric oxide (NO.), superoxide anion (O2.-), and the N-methyl-D-aspartate (NMDA) agonist, cysteine. Similarly, macrophages activated by HIV-1 envelope protein gp120 also appear to release arachidonic acid and its metabolites, and cysteine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Update on current models of HIV-related neuronal injury: platelet-activating factor, arachidonic acid and nitric oxide. 787 85


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