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

Reactive oxygen intermediates (ROI) such as superoxide (O2-), hydrogen peroxide (H2O2) and hydroxyl radicals (.OH) are involved in the pathogenicity of various diseases. There is also evidence that superoxide is involved in disease progression following infection by influenza virus, HIV-1 and human cytomegalovirus (HCMV). Healthy donor-derived peripheral blood monocytes/macrophages, which seem to be the major reservoir for HCMV in vivo, showed significantly higher generation of O2- after HCMV infection. The importance of O2- in cytomegalovirus pneumonitis was also supported in a mouse model system using mouse cytomegalovirus. In addition, the importance of HCMV-induced ROI was also shown in the restenosis and atherosclerosis of smooth muscle cells. This review highlights the relationship between HCMV infection and ROI.
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PMID:[Superoxide generation and human cytomegalovirus infection]. 946 68

Hemodialysis vascular access-related problems account for most hospitalizations in chronic hemodialysis patients. Although some co-morbid risk factors for early fistula failures have been described, a great deal of unknown exists as to why access survival is favorable in some patients. In this longitudinal study, fistulae patency and thrombosis episodes were monitored from placement date in three groups of end-stage renal disease (ESRD) patients who have been on dialysis for > or =90 days. Thirty-six patients (29 male; 80%) with a mean age of 42+/-2 years were monitored. The groups consisted of eight patients with biopsy-confirmed focal segmental glomeruloscierosis (FSGS), 13 with acquired immunodeficiency syndrome-related nephropathy (human immunodeficiency virus [HIV]), and 15 with hypertensive ESRD (hypertensive nephrosclerosis [HTN]) who served as controls. Diabetics and patients aged > or =64 years were excluded. Twenty-five of 36 (69%) fistulae were prosthetic (AVG), while 11 (31%) were native (AVF). The FSGS group was more likely to have an AVG (87.5%), while 54% of the HIV group had an AVG. The thrombosis event rate was significantly greater among the FSGS patients (3/patient-year) than the HIV (0.15/patient-year) and HTN (0.5/patient-year) patients (P < 0.0001 and P < 0.002, respectively). The mean thrombosis-free duration for both AVG and AVF among the HIV and HTN groups were 318.5+/-17 days and 311.7+/-22.5 days, respectively. These were significantly greater than in the FSGS group (26.5+/-7 days; P < 0.0001). The cumulative 1-year patency rate for AVG among the HIV and HTN groups was 85% and 65%, respectively, while that of the FSGS group was 0%. Kaplan-Meier hazard analysis showed that all groups were at risk of access thrombosis as time progressed, but the FSGS group had the highest risk of access thrombosis, which began from the date of placement and increased exponentially with time. The increased thrombosis rate among the patients in the FSGS group correlated with their weight (R = 0.8, P = 0.003) and pre-ESRD 24-hour urinary protein excretion (R = 0.9, P = 0.001). The HIV status appeared to confer enhanced hemodialysis access survival. This may be related to the high rate of native fistulae placement and favorable vascular reactivity to shear stress. Accelerated atherosclerosis and small caliber vessels may be responsible for the poor fistulae outcome among the FSGS group. More studies will be necessary to further explore these findings.
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PMID:Hemodialysis vascular access: variable thrombus-free survival in three subpopulations of black patients. 946 95

beta-chemokines play an important role in the development of immunologic reactions. Macrophages are major beta-chemokine-producing cells during T-cell directed, delayed-type hypersensitivity reactions in tissues, and have been reported to be important producers of beta-chemokines in the lymph nodes of HIV-1-infected individuals. However, the physiological signals responsible for inducing macrophages to produce beta-chemokines have not been established. Two soluble T cell products, interferon-gamma and granulocyte-macrophage colony stimulating factor, were added to cultured macrophages, but failed to stimulate the production of macrophage inflammatory protein-1alpha and -1beta; regulated upon activation, normal T cell expressed and secreted (RANTES); or monocyte chemoattractant protein-1. Instead, direct cell-cell contact between macrophages and cells engineered to express CD40L (also known as CD154) resulted in the production of large amounts of macrophage inflammatory protein-1alpha and -1beta, and RANTES (all ligands for CCR5), and monocyte chemoattractant protein-1 (a ligand for CCR2). Supernatants from CD40L-stimulated macrophages protected CD4(+) T cells from infection by a nonsyncytium-inducing strain of HIV-1 (which uses CCR5 as a coreceptor). These results have implications for granulomatous diseases, and conditions such as atherosclerosis and multiple sclerosis, where CD40L-bearing cells have been found in the macrophage-rich lesions where beta-chemokines are being produced. Overall, these findings define a pathway linking the specific recognition of antigen by T cells to the production of beta-chemokines by macrophages. This pathway may play a role in anti-HIV-1 immunity and the development of immunologic reactions or lesions.
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PMID:CD40 ligand (CD154) stimulation of macrophages to produce HIV-1-suppressive beta-chemokines. 956 Feb 54

Accumulating data from a number of laboratories have recently indicated that the response of transcription factor NF-kappaB to alterations in the redox homeostasis of cells may play an important role in modulating immune function. The activation of NF-kappaB has been recognized to regulate a number of genes necessary for normal T cell responses including IL-2, IL-6, IL-8, and several T cell surface receptors. Diminished NF-kappaB activity has been shown to occur in T cells with aging, suggesting that impaired activation of NF-kappaB might occur during cellular senescence. In addition, aberrancies in NF-kappaB activity have been implicated in the immunopathogenesis of diseases involving immune or inflammatory processes such as atherosclerosis and HIV-1 infection. The role of H2O2 and other reactive oxygen species (ROS) as an integratory secondary messenger for divergent T cell signals has been complicated by the fact that various T cell lines and peripheral blood T cells differ markedly in the levels of NF-kappaB activation induced by oxidant stress. Additionally, proposed pathways of NF-kappaB activation have been based on indirect evidence provided by experiments which used antioxidants to inhibit active NF-kappaB formation. Further, complete activation of T cells requires at least two signals, one that stimulates an increase in intracellular calcium and one that stimulates enzymatic processes including kinases. Similarly, substantial evidence indicates that full activation of NF-kappaB requires dual signals. The ability of H2O2 or other ROS to induce T cell signals and functional responses by these two mechanisms is reviewed and the specific response of NF-kappaB to redox changes in T cells is examined. Data are also presented to suggest that the redox regulation in NF-kappaB activation may be relevant to immune-related diseases and to aging.
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PMID:Redox signals and NF-kappaB activation in T cells. 968 Jan 81

Chemokines are proinflammatory cytokines that function in leukocyte chemoattraction and activation and have recently been shown to block the HIV-1 infection of target cells through interactions with chemokine receptors. In addition to their function in viral disease, chemokines have been implicated in the pathogenesis of atherosclerosis. Expression of the CC chemokine monocyte chemoattractant protein-1 (MCP-1) is upregulated in human atherosclerotic plaques, in arteries of primates on a hypercholesterolaemic diet; and in vascular endothelial and smooth muscle cells exposed to minimally modified lipids. To determine whether MCP-1 is causally related to the development of atherosclerosis, we generated mice that lack CCR2, the receptor for MCP-1 (ref. 7), and crossed them with apolipoprotein (apo) E-null mice which develop severe atherosclerosis. Here we show that the selective absence of CCR2 decreases lesion formation markedly in apoE-/- mice but has no effect on plasma lipid or lipoprotein concentrations. These data reveal a role for MCP-1 in the development of early atherosclerotic lesions and suggest that upregulation of this chemokine by minimally oxidized lipids is an important link between hyperlipidaemia and fatty streak formation.
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PMID:Decreased lesion formation in CCR2-/- mice reveals a role for chemokines in the initiation of atherosclerosis. 973 72

Patients infected with HIV are at increased risk of atherosclerosis, and have evidence of endothelium dysfunction. The hypothesis was tested that HIV-related endothelium dysfunction is related to loss of antioxidants. This was done by the supplementation of the antioxidants selenium and beta-carotene. We supplemented the diet of 10 HIV-seropositive subjects with 100 microg selenium daily, 11 subjects with 30 mg beta-carotene twice daily while 15 subjects were not supplemented. Plasma was obtained at outset and after a year, and tested by ELISA for endothelial cell, platelet and inflammatory markers. The non-supplemented patients experienced increases in von Willebrand factor and soluble thrombomodulin (both p <0.01). There were no changes in any of the indices in the patients taking selenium or beta-carotene. Increased von Willebrand factor and soluble thrombomodulin in the non-supplemented patients imply increased damage to the endothelium over the year of the study. Therefore we interpret the lack of increase in the patients taking antioxidants as evidence of the protection of the endothelium by these agents.
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PMID:Effect of the antioxidants selenium and beta-carotene on HIV-related endothelium dysfunction. 986 76

Probiotics are specific products of microorganisms, and by being biologically active positively act on stabilizing the bacteriological flora of the gastrointestinal tract. They are live or lyophilized bacterial cultures, especially those derived from lactic fermentation (Lactobacillacea and Streptococcacea). The first to use the term probiotics were Lilly and Stillwell in 1965 when referring to substances produced by protozoa, which in turn stimulated the growth of other organisms. Probiotics are devoid of side affects and do not cause accumulation of toxic substances in the body. They are administered for therapeutic, prophylactic and nutritional purposes both in humans and in animals. Interest into probiotics has been spurred on by the growing abundance of civilization disorders such as neoplasms, atherosclerosis, heart disease, hypertension and HIV infection. Probiotics are potentially capable of annihilating these disorders. Starter cultures are pure mixed bacterial, fungal or mold cultures which by transformation of their metabolism faciliate favourable changes in apperance, aroma, consistency, and durability of foodstuffs. Contemporary knowledge concerning probiotics and their action is derived from many years of tradition in consumption of fermented milk products and the documentation of much research into strains of lactic bacteria, their harmless action on health and overall beneficial effect.
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PMID:[Probiotics and their therapeutic properties]. 1044 11

Thanks to progress in zinc research, it is now possible to describe in more detail how zinc ions (Zn++) and nitrogen monoxide (NO), together with glutathione (GSH) and its oxidized form, GSSG, help to regulate immune responses to antigens. NO appears to be able to liberate Zn++ from metallothionein (MT), an intracellular storage molecule for metal ions such as zinc (Zn++) and copper (Cu++). Both Zn++ and Cu++ show a concentration-dependent inactivation of a protease essential for the proliferation of the AIDS virus HIV-1, while zinc can help prevent diabetes complications through its intracellular activation of the enzyme sorbitol dehydrogenase (SDH). A Zn++ deficiency can lead to a premature transition from efficient Th1-dependent cellular antiviral immune functions to Th2-dependent humoral immune functions. Deficiencies of Zn++, NO and/or GSH shift the Th1/Th2 balance towards Th2, as do deficiencies of any of the essential nutrients (ENs) - a group that includes methionine, cysteine, arginine, vitamins A, B, C and E, zinc and selenium (Se) - because these are necessary for the synthesis and maintenance of sufficient amounts of GSH, MT and NO. Via the Th1/Th2 balance, Zn++, NO, MT and GSH collectively determine the progress and outcome of many diseases. Disregulation of the Th1/Th2 balance is responsible for autoimmune disorders such as diabetes mellitus. Under Th2, levels of interleukin-4 (II-4), II-6, II-10, leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) are raised, while levels of II-2, Zn++, NO and other substances are lowered. This makes things easier for viruses like HIV-1 which multiply in Th2 cells but rarely, if ever, in Th1 cells. AIDS viruses (HIVs) enter immune cells with the aid of the CD4 cell surface receptor in combination with a number of co-receptors which include CCR3, CCR5 and CXCR4. Remarkably, the cell surface receptor for LTB4 (BLTR) also seems to act as a co-receptor for CD4, which helps HIVs to infect immune cells. The Th2 cytokine II-4 increases the number of CXCR4 and BLTR co-receptors, as a result of which, under Th2, the HIV strains that infect immune cells are precisely those that are best able to accelerate the AIDS disease process. The II-4 released under Th2 therefore not only promotes the production of more HIVs and the rate at which they infect immune cells, it also stimulates selection for the more virulent strains. Zn++ inhibit LTB4 production and numbers of LTB4 receptors (BLTRs) in a concentration-dependent way. Zn++ help cells to keep their LTB4 'doors' shut against the more virulent strains of HIV. Moreover, a sufficiency of Zn++ and NO prevents a shift of the Th1/Th2 balance towards Th2 and thereby slows the proliferation of HIV, which it also does by inactivating the HIV protease. Research makes it look likely that deficiencies of ENs such as zinc promote the proliferation of Th2 cells at the expense of Th1 cells. Zinc deficiency also promotes cancer. Under the influence of Th1 cells, zinc inhibits the growth of tumours by activating the endogenous tumour-suppressor endostatin, which inhibits angiogenesis. The modern Western diet, with its excess of refined products such as sugar, alcohol and fats, often contains, per calorie, a deficiency of ENs such as zinc, selenium and vitamins A, B, C and E, which results in disturbed immune functions, a shifted Th1/Th2 balance, chronic (viral) infections, obesity, atherosclerosis, autoimmunity, allergies and cancer. In view of this, an optimization of dietary composition would seem to give the best chance of beating (viral) epidemics and common (chronic) diseases at a realistic price.
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PMID:Modern diets and diseases: NO-zinc balance. Under Th1, zinc and nitrogen monoxide (NO) collectively protect against viruses, AIDS, autoimmunity, diabetes, allergies, asthma, infectious diseases, atherosclerosis and cancer. 1049 17

A review on participation of chlamydiae in the origin of the HIV-infection, carcinoma and atherosclerosis. The antibodies against the newly discovered pgp3 protein of C. trachomatis were found in 83-87% of the seropositive HIV patients. The participation of C. trachomatis in the etiology of cervical and ovarian carcinoma has been discussed in a number of articles. Simultaneous examinations along different lines allow the hypothesis, that C. trachomatis acts as a cofactor in the development of ovarian and cervical carcinoma. Chronic infection by C. pneumoniae appears to be one of the risk factors of pulmonary carcinoma. Many papers dealing with the relation of chlamydiae and atherosclerosis have been published. The relation between the chronic C. pneumoniae-infection and atherosclerosis has been assessed serologically and by direct demonstration of chlamydiae in atheromatous plaques.
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PMID:[Chlamydiae--still new surprises]. 1056 17

Thrombosis of upper extremity arteries is most commonly due to atherosclerosis of the proximal subclavian artery, trauma, or catheter-related injury. In the absence of an identifiable cause, a search for a hypercoagulable state is indicated. Hematologic manifestations of human immunodeficiency virus (HIV) infection and AIDS are frequent occurrences (Coyle TE. Med Clin N Am 1997;81:449-476). The most important of these are cytopenias (anemia, neutropenia, and thrombocytopenia). The incidence and severity of cytopenia are generally correlated to the stage of the HIV infection. In addition, various coagulation abnormalities have been reported in HIV-infected patients. Apart from thrombocytopenia, these have included a prolonged APTT due to the presence of lupus anticoagulant, an increased prevalence of protein S and heparin cofactor II deficiency, and hypoalbuminemia-related fibrin polymerization defects (Toulon P. Ann Bio Clin (Paris) 1998;56:153-160). HIV infection has also been associated with endothelial dysfunction. Although for the most part asymptomatic, elevated D-dimer levels have been found in HIV-infected patients, suggesting the existence of a prethrombotic state. In fact, clinical thrombosis eventuates in 2% of these patients (Toulon, 1988). Documented thromboses have involved both veins and arteries. We hereby present a patient who developed an acute thrombosis of his brachial artery as the initial manifestation of HIV infection.
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PMID:Acute brachial artery thrombosis as the initial manifestation of human immunodeficiency virus infection. 1081 96


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