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

Nineteen colorectal biopsy specimens, stained by Hematein-Eosin-Safran (HES), were examined by light microscopy and showed a thick, blue and fuzzy brush border. Without any further microbiologic investigation, this histologic feature is considered strongly suggestive of colorectal spirochetosis. Our study concerned 19 male patients aged between 35 and 68 years, who had no risk factor for HIV infection, but who belonged to these three groups: (a) those suffering from chronic diarrhea; (b) those without intestinal symptoms; (c) those who had a colonic tumor removed. Rectal biopsy specimens were also taken from a control group of 35 patients seropositive for HIV-1. This thickening, which measured 3-7 microns, showed some variation within the same patient but did not depend on the site of the biopsy. It appeared as a blue fuzzy band on HES stain, was purple on Periodic-Acid-Schiff stain and basophilic after Giemsa stain. Silver stain by Warthin-Starry method confirmed the presence in three cases of numerous spirochetes attached to the epithelial surface. Two of the three patients had no symptom. In the control group, a thickening of the brush border, was observed in only one case, but no spirochete by silver stain was seen. The thickened blue, fuzzy brush border of the colonic mucosa is not a specific criterion. The pathologist must be aware of the possible presence of spirochetes that can only be confirmed by a silver stain. The pathogenicity of spirochetosis remains to be defined.
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PMID:[Colo-rectal spirochetosis: is it an anatomo-pathologic entity?]. 170 40

This work tests the hypothesis that chronic alcohol intoxication suppresses the microbicidal activity of Kupffer cells by modulating the expression of cell surface receptors associated with respiratory burst and the release of potent microbicidal agents [i.e., reactive oxygen species (ROS)]. Because alcohol is also a potential risk factor in human immunodeficiency virus-1 (HIV-1) infection, this study examines the effect of HIV-1 glycoprotein 120 (gp120)-induced ROS release by isolated Kupffer cells. After 16 weeks of ethanol feeding, Kupffer cells from male Sprague-Dawley rats were isolated and assayed for HIV-1 gp120-induced superoxide release. Fluorescein isothiocyanate (FITC)-HIV-1 gp120 binding, NADPH oxidase, and protein kinase C activity in Kupffer cells were measured. Results show that HIV-1 gp120 induced the release of superoxide anion in a dose-dependent manner in normal rats. Mannosylated-bovine serum albumin inhibited FITC-HIV-1 gp120-mediated superoxide release in normal Kupffer cells by 85%. Moreover, 83 +/- 6% of Kupffer cells were FITC-HIV 1 gp120-positive, whereas <30% were CD4-positive. In alcohol-fed rats, HIV-1 gp120-induced ROS release was reduced by 70% and FITC-HIV-1 gp120 binding (in terms of fluorescence intensity per 10[6] Kupffer cells) by 44% in Kupffer cells, without any change in percent positive cells for this ligand. Concomitantly, HIV-1 gp120-induced translocation of NADPH oxidase to the plasma membranes of Kupffer cells in alcohol-fed rats was suppressed by 60%. In contrast, alcohol consumption significantly increased total protein kinase C activity and phorbol ester-induced superoxide release by Kupffer cells. These studies demonstrate that Kupffer cells are likely targets of HIV-1 whose binding sites on macrophages could also include mannose-specific receptors. These observations further suggest that suppression of HIV-1 gp120-mediated ROS production in chronic alcoholics is due to altered cell surface receptor expression for gp120, and defective postreceptor signaling mechanisms, which in turn could lead to attenuated microbicidal activity of hepatic macrophages.
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PMID:Chronic alcohol intoxication attenuates human immunodeficiency virus-1 glycoprotein 120-induced superoxide anion release by isolated Kupffer cells. 958 56

Kidneys from 55 cases (20 with HIV infection and 35 with AIDS) were studied by routine Haematoxylin and Eosin stains and special stains (PAS, PASM GMS, ZN, Mucicarmine and Congo red) to evaluate, glomerular, interstitial and vascular pathology. Twenty-four of the 35 (68.6%) cases of AIDS showed infective aetiology which included 17 cases (48.5%) of tuberculosis, 5 cases (14.4%) of fungal infection (3 cryptococcus neoformans and 2 candida species) and 2 cases (5.7%) of CMV infection. Other lesions noted were amyloidosis and tubular calcinosis. HIV associated nephropathy (HIVAN) was not detected in any of the cases. Intravenous drug abuse was not a risk factor in our cases which probably explains the absence of HIV associated nephropathy in the present study.
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PMID:Renal lesions associated with AIDS--an autopsy study. 1042 Jun 86

The HIV-1 Tat protein, essential for HIV-1 gene expression and viral replication, is known to be secreted by infected cells and has pleiotropic effects on various cell functions. It seems that extracellular Tat may exert its functions on cellular targets by at least two different mechanisms, namely, by adsorptive endocytosis, and by a possible interaction with cell surface receptor(s). Here we report that extracellular Tat activates AIM/CD69 gene transcription through an NF-kappaB-dependent pathway in the erythroleukemia cell line K562. Tat induces NF-kappaB binding to DNA as a result of IkappaBalpha phosphorylation and degradation, which depend on the intracellular redox state. We found that the second Tat-coding exon is required for CD69 gene trans-activation, but not for HIV LTR gene transcription. Fluorescein-labeled Tat proteins were used to study cell surface binding sites and cellular uptake of the proteins. Full-length Tat protein has specific binding sites on the surface of K562 cells, whereas truncated Tat1-48, which is efficiently internalized by the cells, does not bind to the cell surface. Our results suggest that extracellular Tat may activate a cell surface-mediated pathway that induces intracellular signal transduction in K562 cells, leading to the activation of NF-kappaB and the transcription of NF-kappaB-dependent genes, such as CD69.
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PMID:Extracellular HIV type 1 Tat protein induces CD69 expression through NF-kappaB activation: possible correlation with cell surface Tat-binding proteins. 1048 Jun 34

A 32 year old HIV sero positive male patient reported to the Ragas Dental College Annexure at Voluntary Health Services Hospital, Chennai for evaluation of oral health status. He had no history of any drug or tobacco usage. Intra oral examination revealed pigmentation in the buccal mucosa on both sides, which was increasing over the past six months. Histopathologic evaluation of the hyper pigmented lesion was done, using routine Haematoxylin & Eosin and Masson-Fontana stains. The hyper pigmentation was observed to be as a result of increased melanin production in the epithelium. The pathogenesis of hypermelanosis intra-orally in HIV sero-positive patients is discussed in this article.
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PMID:Intra-oral hypermelanosis in an HIV sero-positive patient--a case report. 1470 59

A simple, rapid, sensitive and specific reversed-phase high performance liquid chromatographic (RP-HPLC) method involving ultraviolet detection (lambda = 210 nm) was developed for analysis of indinavir along with propranolol in samples obtained from ex vivo intestinal permeability studies. Chromatography was carried out on C-18 column with mobile phase comprising of phosphate buffer-acetonitrile (68:32, v/v) pumped at flow rate of 1 ml/min. The proposed method has a short run time of 12 min and involves a simple sample preparation for the purpose of reducing permeability model artifacts and to concentrate the samples. Fluorescein was used as internal standard. The proposed method has been validated with regard to specificity, detection limit, recovery, accuracy and precision. For both the drugs, method was found to be selective, linear (R(2) approximately 0.999), accurate (recovery = 100-105%) and precise (<3% R.S.D.) in the range of 2-20 microg/ml. The limit-of-detection and limit-of-quantification of the method were 40 ng/ml and 100 ng/ml for indinavir, and 30 and 80 ng/ml for propranolol, respectively. Indinavir, a widely prescribed HIV protease inhibitor, suffer from bioavailability problems where involvement of P-glycoprotein mediated drug efflux may play a significant role. The proposed method was successfully applied for intestinal permeability of indinavir to estimate the contribution of P-glycoprotein in limiting its oral bioavailability. The advantage of the developed method lies in the simultaneous determination of propranolol, a passive integrity marker, routinely employed in permeability studies and its selectivity in presence of various P-gp modulators and permeability markers.
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PMID:Reversed-phase liquid chromatography with ultraviolet detection for simultaneous quantitation of indinavir and propranolol from ex-vivo rat intestinal permeability studies. 1517 39

The trans-activation response (TAR) RNA stem-loop that occurs at the 5' end of HIV RNA transcripts is an important antiviral target and is the site of interaction of the HIV-1 Tat protein together with host cellular factors. Oligonucleotides and their analogues targeted to TAR are potential antiviral candidates. We have investigated a range of cell penetrating peptide (CPP) conjugates of a 16mer peptide nucleic acid (PNA) analogue targeted to the apical stem-loop of TAR and show that disulfide-linked PNA conjugates of two types of CPP (Transportan or a novel chimeric peptide R6-Penetratin) exhibit dose-dependent inhibition of Tat-dependent trans-activation in a HeLa cell assay when incubated for 24 h. Activity is reached within 6 h if the lysosomotropic reagent chloroquine is co-administered. Fluorescein-labelled stably-linked conjugates of Tat, Transportan or Transportan TP10 with PNA were inactive when delivered alone, but attained trans-activation inhibition in the presence of chloroquine. Confocal microscopy showed that such fluorescently labelled CPP-PNA conjugates were sequestered in endosomal or membrane-bound compartments of HeLa cells, which varied in appearance depending on the CPP type. Co-administration of chloroquine was seen in some cases to release fluorescence from such compartments into the nucleus, but with different patterns depending on the CPP. The results show that CPP-PNA conjugates of different types can inhibit Tat-dependent trans-activation in HeLa cells and have potential for development as antiviral agents. Endosomal or membrane release is a major factor limiting nuclear delivery and trans-activation inhibition.
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PMID:Cell-penetrating peptide conjugates of peptide nucleic acids (PNA) as inhibitors of HIV-1 Tat-dependent trans-activation in cells. 1632 67

Peptides based on the amino (N) and carboxy (C)-terminal regions of human immunodeficiency virus type-1 (HIV-1) protease and on the C-terminus of p6* can inhibit HIV-1 protease activity by preventing dimerization. We developed a peptide dimerization inhibitor, P27, that included these domains and a cell permeable domain derived from HIV-1 Tat. P27 inhibited wild type (WT) and protease inhibitor (PI)-resistant HIV-1 protease (IC50: 0.23-0.32 microM). Kinetic and biochemical assays confirmed that P27 inhibits protease dimerization. Fluorescein-labeled peptide accumulated in MT-2 cells and protected acutely infected MT-2 cells from HIV-1-induced cytotoxicity (IC50: 5.1 microM). P27 also inhibited p24 accumulation from H9 and U937 cells chronically infected with WT or PI-resistant HIV-1. Immunoblot analysis on the supernatants and infected cells revealed a block in virus release by P27 rather than an inhibition of polyprotein processing. However, inhibition of p55 Gag processing by active-site inhibitors was enhanced when combined with P27, suggesting that P27 can affect protease function in maturing virions. Although P27 was rationally designed to block dimerization of the mature HIV-1 protease, the effects of P27 on HIV-1 replication may be related to partial inhibition of Gag-Pol processing leading to a disruption in virus release.
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PMID:Inhibition of HIV-1 replication by a peptide dimerization inhibitor of HIV-1 protease. 1668 79

Two groups of the antiviral agents: 1) adamantane- and norbornen-containing compounds with in-built cholesterol to potentiate the membranotropic properties and 2) synthetic matrix protein peptides (peptides A and B) were found to have effects on HIV replication. The agents of the former group produced antiviral activity only when added in combination with the virus. Peptide A (matrix protein 43-60 amino acids) inhibited viral replication when added in both the early and late periods. Fluorescein-labeled peptide A was detectable in the cytoplasm and nucleus (although adsorption of a portion of the peptides cannot be excluded onto the cell surface). Peptide A was shown to inhibit Gag precursor p55 transport from the nuclei to the plasma membrane, the site of virus assembly. Peptide B had no antiviral activity.
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PMID:[Effects of novel antiviral agents on HIV-1 replication]. 1945 9

Integration of the DNA copy of the genomic RNA into an infected cell genome is one of the key steps of the replication cycle of all retroviruses. It is catalyzed by the viral enzyme, integrase. We have shown that conjugates of short single-stranded oligonucleotides with eosin efficiently inhibit the catalytic activity of the HIV-1 integrase. In this article, we have found that the dependence of the integrase catalytic activity on the concentration of oligonucleotides has a bell-shaped pattern. The modulation of HIV-1 integrase activity correlated with the oligonucleotide length and was not associated with specific sequences. Moreover, a similar mode of the oligonucleotide action was found for integrase from the prototype foamy virus. This dual effect of the oligonucleotide and their conjugates with eosin might be explained by their binding with retroviral integrase in two different sites; the oligodeoxynucleotide binding in the first site results in integrase activation, whereas interactions with another one lead to inhibition of the enzyme activity. Eosin coupling to oligonucleotides did not change the mode of their action but enhanced their affinity to both binding sites. The affinity increase was found to be much more important for the site responsible for the integrase inhibition, thus explaining the high inhibitory potency of oligonucleotide-eosin conjugates.
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PMID:Modulation of HIV-1 integrase activity by single-stranded oligonucleotides and their conjugates with eosin. 2188 54


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