Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transmission of infectious agents from a patient to the following one in the medical office may result from infected collyria, from contact to the cornea by infected instruments or simply by the hands of the medical staff if some rules of hygiene are not respected. The prevention comprises the instillation without contact of the collyria, the adequate disinfection of instruments and the frequent hand washing. The disinfection of the tonometers and contact glasses aims particularly the elimination of viruses. If the virus of herpes, hepatitis and acquired immunodeficiency are eliminated by hypochlorite, oxygenated water and alcohol after 10 minutes, the adenovirus which is not coated is on the other hand resistant to alcohol and may survive several days on instruments. Ideally the disinfection would have to be performed between each utilization by soaking in bleach water at 500 ppm, or in chloramine 0.5%, or in hydrogen peroxide 3% (during 10 minutes). The alcohol may damage the glue of diagnostic contact lens. The hypochlorite attacks the metal. In case of possible contact with the blood of the patient, the wear of gloves is counseled (for example for fluorescein angiography) and is of course mandatory for surgical procedures in the office like excision of chalazion or keratotomy. Disposable needles will be thrown in solid wall containers reserved to this aim without being recapped.
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PMID:[Prevention of infections in the ophthalmology office]. 902 12

Reactive oxygen species (ROS) such as hydrogen peroxide serve as second messengers in the induction of the transcription factor NF-kappaB, and hence in the activation and replication of human immunodeficiency virus type 1 (HIV-1) in human cells. During inflammatory reactions, many oxidative species are produced, one of which is hypochlorous acid (HOCl), which is responsible for the microbicidal effects of activated human polymorphonuclear leukocytes. Treatment of a T-lymphocytic cell line with micromolar concentrations of HOCl promoted the appearance of transcription factor NF-kappaB (the heterodimer p50/p65) in the nucleus of the cells, even in the absence of de novo protein synthesis. Western blot analysis of the NF-kappaB inhibitory subunits (IkappaB) demonstrated that both IkappaB-alpha proteolysis and p105 processing were induced by the treatment. NF-kappaB activation was very effective when cells were subjected to hyperthermia before being treated with HOCl. Various antioxidants, such as pyrrolidine dithiocarbamate, p-bromophenacyl-bromide and nordihydroguaiaretic acid could strongly reduce NF-kappaB translocation, demonstrating the importance of oxidative species in the transduction mechanism. Moreover, ACH-2 cells treated with HOCl or H2O2 released tumour necrosis factor-alpha (TNF-alpha) in the supernatants. The importance of TNF-alpha release in NF-kappaB induction by HOCl or H2O2 was demonstrated by the fact that: (1) the nuclear appearance of NF-kappaB was promoted in untreated cells; and (2) synergism between TNF-alpha and HOCl was detected. Collectively, these results suggest that HOCl should be considered as an oxidative species capable of inducing NF-kappaB in a T-lymphocytic cell line through a transduction mechanism involving ROS, and having a long-distance effect through subsequent TNF-alpha release.
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PMID:Activation of the NF-kappaB transcription factor in a T-lymphocytic cell line by hypochlorous acid. 903 66

The tethered-dimer protease of human immunodeficiency virus 1 (HIV-1) [Cheng Y.-S. E., Yin, F.H., Foundling, S., Blomstrom, D. & Kettner, C. A. (1990) Proc. Natl Acad. Sci. USA 87, 9660-9664] and its mutants containing amino acid substitutions or deletions or both in only one flap region were expressed in Escherichia coli. These mutant enzymes showed various degrees of self-processing and significantly reduced catalytic activity toward oligopeptide substrates compared with the wild type. Kinetic parameters determined for one of the oligopeptide substrates showed a dramatic increase in K(m) and decrease in Kcat values. Unexpectedly, the substrate cleavage was more efficient in low salt concentration for a mutant containing a shortened hydrophilic flap. Assays with oligopeptides representing naturally occurring cleavage sites or oligopeptides containing single amino acid substitutions at the P2 and P2' substrate positions showed only moderate changes in the substrate specificity of the mutant proteases. Predicted structures for the mutants were constructed by molecular modeling and used to interpret the results of kinetic measurements. In general, the data suggest that the mutated part of the flaps does not have a major role in determining substrate specificity; rather, it provides the hydrophobic environment and hydrogen-bond interactions with the conserved water that are necessary for efficient substrate binding and catalysis.
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PMID:Activity of tethered human immunodeficiency virus 1 protease containing mutations in the flap region of one subunit. 906 69

Programmed cell death (apoptosis) of T-lymphocytes observed in human immunodeficiency virus (HIV) infected individuals could be linked to oxidative stress. Therefore, we have investigated whether reactive oxygen species (ROS) induce apoptosis, which might contribute to the cell loss during progression of HIV-1 infection. ROS were generated in peripheral blood mononuclear cells (PBMC) obtained from HIV-1-positive patients and from healthy controls by stimulation with bacteria or by treatment with hypoxanthine/xanthine oxidase, which has been shown to generate ROS without direct involvement of cytokines. A dose-dependent inhibition of ROS formation correlated with the reduction of apoptosis induced by both bacterial and hypoxanthine/xanthine oxidase stimulation, suggesting that ROS generation was responsible for the induction of apoptosis. In addition, hydrogen peroxide (H2O2) rather than superoxide (O2.-) was observed to induce apoptosis. ROS-dependent apoptosis was shown to be independent of cytokines such as tumor necrosis factor-alpha (TNF-alpha). ROS-induced apoptosis was significantly enhanced in HIV-infected subjects even in the very early stages after infection. Moreover, ROS-mediated apoptosis was not restricted to a particular lymphocyte subset. In view of the diminished oxidative resistance of HIV-infected individuals, our results suggest that ROS-mediated apoptosis might contribute to the deletion of lymphocytes and to the pathogenesis of the disease.
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PMID:Ex vivo induction of apoptosis in lymphocytes is mediated by oxidative stress: role for lymphocyte loss in HIV infection. 911 45

The trans-activating region (TAR) RNA-Tat protein interaction is important for activation of transciption in the human immunodeficiency virus (HIV). A model complex for this interaction composed of the two base bulge HIV-2 TAR and the amide derivative of arginine was studied by multidimensional heteronuclear NMR. Because of the improved spectral properties of the HIV-2 TAR complex, a larger number of NOEs in the bulge region were observed than in earlier studies of the HIV-1 TAR-argininamide complex. A total of 681 NOE distance restraints were collected and used to determine the solution structure of the HIV-2 TAR-argininamide complex. As observed in the previously proposed model from this lab, the two A-form stems co-axially stack and the critical U23 and the argininamide are located in the major groove. Model calculations including non-experimental restraints indicate that U23 is within hydrogen bonding distance to A27 consistent with the formation of a U x A x U base-triple. Base-triple formation helps open the major groove to increase the accessibility of G26 to hydrogen bond donors from the guanidinium group of argininamide. Argininamide binding is stabilized by stacking of the guanidinium group between the bases of A22 and U23, forming an argininamide sandwich.
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PMID:Solution structure of the HIV-2 TAR-argininamide complex. 912 42

Feline immunodeficiency virus, like human immunodeficiency virus type 1, is a retrolentivirus causing neurological disease and immune suppression. Primary neurological complications, including human immunodeficiency virus encephalopathy and peripheral neuropathy, and neuropathological changes, including gliosis, neuronal injury and multinucleated giant cells, have been described for human immunodeficiency virus type 1 infection. Excitatory amino acids have been implicated as a basis for human immunodeficiency virus encephalopathy and the accompanying neuronal injury. Here, we test our hypothesis that feline immunodeficiency virus infection results in glial activation accompanied by enhanced glutamatergic activity, causing neuronal loss. Neurological signs observed in naturally and experimentally infected animals included ataxia, aggressivity and reduced motor activity. Neuropathological changes included gliosis, perivascular cuffing and neuronal dropout in the brains of both experimentally and naturally infected animals, but not in uninfected animals. Feline immunodeficiency virus antigen and genome were detected in the brains of all experimentally and naturally infected animals. Proton nuclear magnetic resonance spectroscopy revealed significantly increased glutamate levels in the feline immunodeficiency virus-infected animals. In contrast, glutamate decarboxylase levels in GABAergic neurons were reduced in feline immunodeficiency virus-infected animals. These findings provide direct in vivo evidence for enhanced glutamate levels in conjunction with neuronal loss, supporting the hypothesis of glutamate-mediated neurotoxicity as a major mechanism in the neuropathogenesis of retrolentiviral infections.
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PMID:Feline immunodeficiency virus causes increased glutamate levels and neuronal loss in brain. 913 Jul 96

Opportunistic infections often coexist with human immunodeficiency virus (HIV) infection in brain. Making the correct diagnosis is often difficult despite recent advances in neuroimaging techniques. 1H magnetic resonance spectroscopy (1H MRS) is an emerging non-invasive examination for diagnosis and monitoring of brain disorders. 1H MRS measures a variety of organic compounds using magnetism and radio waves. Biochemical aberrations in brain, not shown by conventional tests, may be demonstrated by 1H MRS testing. A patient coinfected with HIV and hepatitis B (HBV) presented with progressive dementia. Clinical, neuroradiological and cerebrospinal fluid (CSF) examinations failed to provide a diagnosis in support of either HIV-1-associated cognitive/motor complex or HBV-induced hepatic encephalopathy (HE), 1H MRS was used in an attempt to discriminate between these diagnoses. Spectroscopy demonstrated increased glutamine and normal N-acetyl aspartate (NAA) levels, metabolic changes consistent with HE. These findings were later confirmed pathologically. Proton magnetic resonance spectroscopy is a non-invasive test with utility for the differential diagnosis of HIV-associated dementia.
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PMID:Utility of cerebral proton magnetic resonance spectroscopy in differential diagnosis of HIV-related dementia. 922 65

The mechanisms by which monocytes from patients infected with human immunodeficiency virus (HIV) have reduced growth inhibitory activity against Cryptococcus neoformans was examined. Monocyte-enriched peripheral blood mononuclear cells from 12 HIV-seropositive donors with CD4 cell counts of 10-210 cells/mm3 (median, 85) and HIV-seronegative donors were compared in assays to determine the binding and phagocytosis of C. neoformans and the respiratory burst and degranulation in response to C. neoformans and zymosan. Monocytes from HIV-infected and uninfected persons bound and ingested C. neoformans equally well; however, generation of hydrogen peroxide and specific release of beta-glucuronidase in response to C. neoformans was significantly reduced in monocyte-enriched cells from the HIV-infected donors. The impaired anticryptococcal activity of monocytes from persons with HIV may be related to defects in both oxidative and nonoxidative effector pathways that occur after the binding and internalization of the organism.
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PMID:Mechanisms of impaired anticryptococcal activity of monocytes from donors infected with human immunodeficiency virus. 923 27

Crystal structures of complexes of a D30N mutant of feline immunodeficiency virus protease (FIV PR) complexed with a statine-based inhibitor (LP-149), as well as with a substrate based on a modification of this inhibitor (LP-149S), have been solved and refined at resolutions of 2.0 and 1.85 A, respectively. Both the inhibitor and the substrate are bound in the active site of the mutant protease in a similar mode, which also resembles the mode of binding of LP-149 to the native protease. The carbonyl oxygen of the scissile bond in the substrate is not hydrated and is located within the distance of a hydrogen bond to an amido nitrogen atom from one of the two asparagines in the active site of the enzyme. The nitrogen atom of the scissile bond is 3.25 A from the conserved water molecule (Wat301). A model of a tetrahedral intermediate bound to the active site of the native enzyme was built by considering the interactions observed in all three crystal structures of FIV PR. Molecular dynamics simulations of this model bound to native wild-type FIV PR were carried out, to investigate the final stages of the catalytic mechanism of aspartic proteases.
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PMID:Crystal structures of the inactive D30N mutant of feline immunodeficiency virus protease complexed with a substrate and an inhibitor. 927

The carboxyl-terminal domain, residues 146 to 231, of the human immunodeficiency virus-1 (HIV-1) capsid protein [CA(146-231)] is required for capsid dimerization and viral assembly. This domain contains a stretch of 20 residues, called the major homology region (MHR), which is conserved across retroviruses and is essential for viral assembly, maturation, and infectivity. The crystal structures of CA(146-231) and CA(151-231) reveal that the globular domain is composed of four helices and an extended amino-terminal strand. CA(146-231) dimerizes through parallel packing of helix 2 across a dyad. The MHR is distinct from the dimer interface and instead forms an intricate hydrogen-bonding network that interconnects strand 1 and helices 1 and 2. Alignment of the CA(146-231) dimer with the crystal structure of the capsid amino-terminal domain provides a model for the intact protein and extends models for assembly of the central conical core of HIV-1.
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PMID:Structure of the carboxyl-terminal dimerization domain of the HIV-1 capsid protein. 934 81


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