Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The implication of blood in HIV and other viruses transmission has invigorated the research for finding a fluid able to replace blood as regards its oxygen-carrying properties. In this work, the specifications of a potential substitute are first defined. Then, the means to be developed in order to match these specifications at best are precise. Afterwards, a possible oxygen-carrier, the hemoglobin-dextran-BTC conjugate, is described.
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PMID:[Extracted hemoglobins as oxygen transporters: proposal of a hemoglobin-dextran-benzenetetracarboxylate conjugate]. 768 13

Apoptosis or programmed cell death (PCD) is a type of death occurring in various physiological processes. Several data suggest that: (1) apoptosis may play a critical role in AIDS pathogenesis; (2) an increase of endocellular free radical levels can be associated with activation of previously latent HIV virus. Tumor necrosis factor (TNF), a cytokine capable of inducing oxygen free radicals and apoptosis, appears also to be involved in HIV activation. The present findings, which elucidate a relationship between the percentage of apoptotic cells, reduced glutathione (GSH) depletion and an increase of p24 antigenemia, suggest that pretreatment with N-acetylcysteine (NAC) is capable of decreasing the above-mentioned phenomena in HIV-infected U937 cells.
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PMID:N-acetylcysteine inhibits apoptosis and decreases viral particles in HIV-chronically infected U937 cells. 768 66

Infection with a sexually transmitted disease (STD) increases the risk for human immunodeficiency virus (HIV) infection. Polymorphonuclear leukocytes (PMNs) are recruited into the genital tract by STD pathogens, such as Chlamydia trachomatis. Semen of HIV-infected men contains HIV associated with mononuclear cells. This study investigated the interaction among PMNs from HIV-uninfected persons, C. trachomatis, and HIV-infected cells and examined the mechanisms for enhanced HIV replication. We demonstrated that PMNs from HIV-seronegative donors induced HIV replication in mononuclear cells from 17 HIV-infected patients in medium without exogenous IL-2. HIV in the cell-free supernatants from cocultures of PMNs and patients' peripheral blood mononuclear cells (PBMCs) was replication competent, as indicated by their capacity to propagate HIV in a second round of culture using PBMCs from HIV-seronegative individuals and by the fact that proviral DNA was found in these cells. PMNs from HIV-seronegative donors increased HIV replication over 100-fold in chronically HIV-infected cell lines of the monocytic, T, and B cell lineages. Moreover, PMNs increased U1 cells' production of p24 antigen by as much as ninefold when compared with U1 cells cocultured with PBMCs. The addition of C. trachomatis to PMN and U1 coculture increased HIV replication by an additional ninefold at 24 h, whereas C. trachomatis alone had no effect on p24 antigen production by U1 cells. Thus, C. trachomatis serves not only to recruit PMNs, but also to interact with PMNs to increase HIV replication. HIV replication is triggered by contact of HIV-infected cells with PMNs, by the generation of reactive oxygen intermediates (ROIs), and by soluble factors such as TNF-alpha and IL-6. This is based on the findings that production of p24 antigen, IL-6, and TNF-alpha induced by PMNs is abrogated by disrupting or partitioning PMNs from HIV-infected cells; is inhibited by superoxide dismutase and catalase, enzymes that destroy ROIs; is enhanced by differentiated HL60 cells capable of producing ROIs; and is induced by PMNs tested negative for CMV. Furthermore, the production of ROIs is independent of HIV infection of mononuclear cells, since PMNs cocultured with HIV-uninfected parental monocytic and T cell lines generated ROIs. Therefore, the increased risk for acquiring HIV infection associated with chlamydia cervicitis may be related to the local recruitment of PMNs by C. trachomatis and the induction of infectious virus from mononuclear cells present in semen. These observations provide a rationale for strategies to reduce HIV transmission by control of STD.
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PMID:Neutrophils from human immunodeficiency virus (HIV)-seronegative donors induce HIV replication from HIV-infected patients' mononuclear cells and cell lines: an in vitro model of HIV transmission facilitated by Chlamydia trachomatis. 769 32

Several recent reports have indicated high levels of reactive oxygen species, causing oxidative stress, in the pathogenesis of HIV infection. Oxidative stress may lead to enhanced HIV replication in infected cells and may also aggravate the immunodeficiency by reduction of cellular immunity and possibly by increased programmed cell death of lymphocytes. Moreover, reduced levels of antioxidants have been found in patients with HIV infection. This raises the question of whether antioxidant therapy might be beneficial in patients with HIV infection. Until now, only a few preliminary, clinical studies have been completed. Further clinical trials are needed to assess the possible role of antioxidants in the treatment of HIV infection.
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PMID:[Can HIV infection be treated with antioxidants?]. 770 93

Reactive oxygen species like hydrogen peroxide (H2O2) have been shown to serve as messengers in the induction of NF-kappa B and then in the activation and replication of HIV-1 in human cells. Because singlet oxygen (1O2) is another very important reactive oxygen species whose action in transcription factor activation is totally undetermined, we started to investigate its role in both NF-kappa B and HIV-1 activation. For provoking unbalanced redox conditions, 1O2 was generated by photosensitization using methylene blue as photosensitizer. Lymphocytes or monocytes (ACH-2 or U1 respectively) latently infected with HIV-1 were treated by photosensitization mediated by methylene blue and the production of reactive oxygen species was monitored through their cytotoxic effect in infected cells. The generation of 1O2 by methylene blue turns out to be very efficient in inducing NF-kappa B as a heterodimer composed of the p50 and p65 subunits. This induction appears specific since other transcription factors like AP-1 are only weakly activated by this treatment. In comparison with other inducing treatments such as phorbol esters or tumor necrosis factor alpha (TNF-alpha), the methylene-blue-mediated activation of NF-kappa B is slow, becoming optimal 180 min after treatment. These kinetic data were obtained by following, on the same samples, both the emergence of NF-kappa B in the nucleus and the disappearance of I kappa B-alpha in the cytoplasmic extracts. Conjugated with the induction of this transcription factor, HIV-1 reactivation from these latently infected cells was also observed by the measurement of reverse transcriptase activity in the cell supernatants. These data allow us to postulate that 1O2 is a biologically important reactive oxygen species which could play a role in the establishment of oxidative stress conditions leading to HIV-1 activation via the presence of NF-kappa B in the nucleus of infected cells.
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PMID:NF-kappa B transcription factor and human immunodeficiency virus type 1 (HIV-1) activation by methylene blue photosensitization. 770 61

We postulated that changes in the cell surface display of molecules that facilitate cell-cell and cell-matrix adhesions may reflect the changing immunosurveillance capacity of blood monocytes during progression of human immunodeficiency virus (HIV) infections. In Centers for Disease Control (CDC) stage A patients, whose monocytes' ability to phagocytose bacteria and generate reactive oxygen intermediates is often increased, the frequency of monocytes expressing CD49d, HLA-DP, HLA-DQ, and an activation epitope of CD11a/CD18 was increased and monocyte transendothelial migration was unimpaired. In CDC stage B/C patients, whose monocytes' ability to phagocytose bacteria and migrate across confluent endothelial monolayers was diminished, surface expression of CD49e and CD62L and the percentage of monocytes expressing CD18, CD11a, CD29, CD49e, CD54, CD58, CD31, and HLA-I were significantly decreased. Incubating normal donor monocytes with immune complexes in vitro reproduced the phenotypic and functional abnormalities seen in stage B/C patients. By contrast, in vitro stimulation with subcellular particulates released by apoptotic lymphocytes reproduced changes seen in stage A patients' monocytes. Although circulating monocytes appear to be activated at all stages, these data suggest that the high levels of circulating immune complexes, found predominantly in the later stages of HIV infection, may be particularly instrumental in reducing the monocyte's capacity to maintain surveillance against infection.
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PMID:Phenotypic and functional changes in peripheral blood monocytes during progression of human immunodeficiency virus infection. Effects of soluble immune complexes, cytokines, subcellular particulates from apoptotic cells, and HIV-1-encoded proteins on monocytes phagocytic function, oxidative burst, transendothelial migration, and cell surface phenotype. 770 78

Recent data suggest that gp120, a glycoprotein secreted by HIV-1-infected macrophages, is neurotoxic, and that toxicity is mediated, at least in part, by overactivation of NMDA-type excitatory amino acid receptors. In experimental animals, considerable evidence indicates that hypoglycemic and ischemic neuronal injury are mediated by endogenous excitatory amino acids. We hypothesized that in the presence of gp120 the severity of brain injury resulting from hypoglycemia and cerebral ischemia would increase. To test this hypothesis in vivo, we evaluated the influence of gp120 on the extent of brain injury resulting from these two clinically relevant pathophysiological insults in 7-day-old (P7) rats, the developmental stage of peak susceptibility to NMDA neurotoxicity. We compared the severity of hippocampal injury resulting from right intrahippocampal injections of gp120 (50 ng) in P7 rats rendered markedly hypoglycemic (n = 10) and in controls (n = 12). We also determined the influence of gp120 administration on the severity of hypoxic-ischemic injury, using a perinatal rat stroke model. P7 rats received intrahippocampal injections of gp120 (50 ng) (n = 23) or saline (n = 18) and then underwent right carotid ligation, followed by 2 h exposure to 8% oxygen. Brain injury was evaluated 5 days later, based on neuropathology evaluation and measurements of bilateral regional cross-sectional areas. The severity of hippocampal injury, based on cross-sectional area measurements, was considerably greater in animals from the hypoglycemic group than in litter-mate gp120-injected controls. Among the animals that underwent hypoxic-ischemic lesioning, the severity of injury, based on histopathology scoring and regional volume measurements, was considerably greater in animals that received gp120 than in those that received saline. These results provide support for the hypothesis that locally secreted HIV peptides, such as gp120, may potentiate the neurotoxicity of endogenous excitatory amino acid neurotransmitters in HIV-infected brain.
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PMID:gp120, an HIV-1 protein, increases susceptibility to hypoglycemic and ischemic brain injury in perinatal rats. 772 Aug 21

Three HIV-infected patients, men of 28 and 43 years old, and a woman of 32 years old, developed cutaneous reactions to one or more drugs prescribed to treat secondary infections. An increased incidence of hypersensitivity reactions to sulfonamides has been reported in literature. HIV-seropositive patients, however, appear to be prone to develop hypersensitivity reactions to many other drugs more often than HIV-seronegative patients. The underlying pathophysiological mechanism is not known. A possible explanation could be a virus-induced altered metabolism leading to an increased production of toxic reactive metabolites or inability either to conjugate these metabolites or to protect tissues against drug induced formation of reactive oxygen species, due to glutathione deficiency. Different serum IgE concentrations and enhanced histamine release of basophilic granulocytes have also been found in HIV-seropositive patients.
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PMID:[Drug reactions occur frequently in patients with HIV infection]. 775 38

A monoclonal antibody for the conservative region of gp41, which is one of the HIV envelope proteins, was produced. The antigen determining site of gp41 was examined using the epitope mapping technique, followed by an enzyme linked immunosorbent assay. Some peptides had comparable affinities for the monoclonal antibody, but the peptide EGIEE, having a slightly weaker immunoaffinity than gp41, was the most preferable for the construction of an immunoaffinity AIDS sensor. For the detection of gp41, EGIEE was labelled with catalase and used as a mimic antigen; it was bound to the antibody present on an immuno-membrane and, due to the replacement reaction of the mimic antigen by gp41, indirect quantitative measurement of gp41 was possible using an oxygen electrode. Anti-gp41 antibody was also detected using a mimic antibody, which was chemically modified with polyethylene glycol. An immunoaffinity AIDS sensor was constructed using the mimic molecules which were tailored to have a suitable immunoaffinity for HIV antigen and/or antibody.
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PMID:An approach for an immunoaffinity AIDS sensor using the conservative region of the HIV envelope protein (gp41) and its monoclonal antibody. 778 71

Between February and April 1991, six adults were admitted to the New York Hospital because of measles pneumonitis. The diagnosis was confirmed by serology and/or viral culture. Uncommon clinical features among patients with this diagnosis included thrombocytopenia, hepatitis, myositis, and hypocalcemia. All patients were markedly hypoxic (initial alveolar--arterial oxygen gradients while the patients were breathing room air, 40-61 mm Hg); four required support with mechanical ventilation. All patients received therapy with intravenous ribavirin (20-35 mg/[kg.d]) for 1 week. The respiratory status of five patients (one of whom was positive for human immunodeficiency virus [HIV]) who were treated early (days 2-5 of illness) promptly improved; all abnormal parameters eventually returned to baseline. Treatment of the sixth patient, who was presumed to be HIV-infected, was initiated on hospital day 22; this patient died of progressive oxygenation failure on day 38. We conclude that life-threatening measles pneumonitis in adults may be more common that previously appreciated, regardless of the patient's immune status. Therapy with intravenous ribavirin was well tolerated by our patients and was associated with reversal of respiratory compromise.
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PMID:Severe measles pneumonitis in adults: evaluation of clinical characteristics and therapy with intravenous ribavirin. 864 18


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