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)

To accurately quantify HIV-1 neutralizing antibody titers in primary human cells, we developed a single round, focus-forming unit (FFU) reduction assay in human peripheral blood mononuclear cells (PBMC). Infected PBMC were enumerated by a reverse ELISPOT technique in which they were incubated under agarose in the presence of a protease inhibitor in anti-p24 antibody-coated microtiter plates. Viral p24, secreted in the immediate vicinity of infected cells and captured by immobilized antibodies, was subsequently stained using gold-labeled anti-p24-antibody and a precipitating silver substrate. The resulting spots were counted visually, without the aid of a microscope, and percent neutralization titers were determined using curve-fitting software. Results of this ELISPOT neutralization assay (ENA) for 15 HIV-positive human specimens were compared with results from a standard PBMC neutralization assay (standard assay) that measured neutralization as a function of p24 concentration by enzyme immunoassay (EIA). The ENA measures FFU reduction of both syncytium-inducing (SI) and non-syncytium-inducing (NSI) primary isolates. Completed assay plates may be retained as a physical record of results or saved as an image using a flat-bed computer scanner.
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PMID:Single-round HIV type 1 neutralization measured by ELISPOT technique in primary human cells. 1621 2

Silver nanoparticles fabricated in Hepes buffer exhibit potent cytoprotective and post-infected anti-HIV-1 activities toward Hut/CCR5 cells.
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PMID:Silver nanoparticles fabricated in Hepes buffer exhibit cytoprotective activities toward HIV-1 infected cells. 1622 Jan 70

In the central nervous system (CNS), HIV-1 targets mainly microglia/macrophages. Like the CD4+ T cell depletion and neuronal loss in AIDS, apoptosis is thought to be involved in eliminating infected macrophages. In this study, we examined the expression of the pro-apoptotic BH3-peptide harakiri (Hrk) in brain tissues of AIDS patients. Immunoreactivity against Hrk was positive in perivascular macrophages infiltrated into some restricted lesions. Most of these immunopositive cells contained small inclusions positive for Grocott's methenamine silver staining. Confocal laser microscopy demonstrated that Hrk expression coincided with immunoreactivities against HIV-1 and Cryptococcus neoformans. Expression of Hrk mRNA was demonstrated in these cells by in situ hybridization, which indicated that Hrk is not phagocytosed material. Some pro-apoptotic bcl-family members, including Hrk, may contribute to the delayed hypersensitive reaction in AIDS, in macrophages eliminating opportunistic infection.
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PMID:The pro-apoptotic human BH3-only peptide harakiri is expressed in cryptococcus-infected perivascular macrophages in HIV-1 encephalitis patients. 1622 49

The vaginal/cervical smears of a group of Moroccan immigrants were used to compare vaginal dysbacteriosis (i.e., a bacterial population change with a decrease in lactobacilli and an increase of coccoid bacteria in vaginal/cervical smears) with Dutch women. From our archives, 779 smears from Moroccan immigrants were compared with 1,060 smears of age-matched Dutch women. For bacterial flora, Jones-Marres silver stains were used to define four groups. Koilocytosis and cervical intraepithelial neoplasia (CIN) were also recorded. The bacterial vaginal flora of Moroccan immigrants and Dutch women was different. The Moroccan women had a lower dysbacteriosis than Dutch women (3% vs. 24%). Koilocytosis and CIN were less frequent in the immigrant population. The possible synergy of a disturbed vaginal flora with human papillomavirus (HPV), HIV, or cervical preneoplasia indicates that vaginal hygiene and a normal flora may have positive effects on the uterine cervix.
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PMID:Dysbacteriosis in silver-stained cervical smears of Dutch-Moroccan immigrants: HPV infection and preneoplasia. 1635 75

The goal of this study is to present the clinical and evolutive features of Pneumocystis infection (PCP) in infants admitted in our clinic. We summarise these aspects from 17 cases (10 male and 7 female infants), admitted between 1st January 2004 and 31st May 2005. PCP infection is rare. It represents 1,5/1000 children (17 cases of 11328 total patients) admitted in our hospital. The risk factors for PCP were age between 6 weeks and 6 months (average 3,38 months) low birth weight (average = 2428 grams), low weight for age, prolonged hospital admission (88,23% of the 17 infants were abandoned in nursery). Only one of them had HIV infection and none presented neoplastic disease. The most prominent clinical aspect was tachypnea (average 78 breath/minute, maximum 130). 16 (94,11%) had difficult breathing with chest in-drawing and flaring of ala nasi. 14 (82,35%) had generalised cyanosis. Only two (11,72%) infants had fever. Radiologic aspects were evocative, with diffuse pulmonary involvement in almost all cases (88,23%). 6 infants (35,29%) had pneumothorax and 2 (11,76%) presented pneumomediastinum. Positive diagnosis was made by microscopic examination of secretions from endotracheal tube aspiration (Grocott methenamine silver stain and Romanowsky stain). 14 infants were ventilated with a good outcome--12 surviving infants (85,7%). All infants had a full course of intravenous Co-trimoxazole. The deceased infants had more risk factors--congenital heart disease 1 case, severe cerebral palsy with organic epilepsy 2 cases. The apparent increase of PCP cases can be related to the number of abandoned children in Romanian pediatric hospitals and nurseries.
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PMID:[Pneumocystis pneumonia in infants]. 1653 25

The human immunodeficiency virus-1 (HIV-1) affects the central nervous system (CNS) in approximately 30% of infected individuals and basal ganglia structures seem to be most affected. The HIV-1-transactivating protein, Tat, has been suggested to be pathogenically relevant in HIV-1-induced neuronal injury. The abuse of methamphetamine (METH), which is great among this patient population, also affects the basal ganglia, causing degeneration of dopaminergic terminals. In previous studies, we demonstrated that coexposure to these two toxins caused a synergistic loss of striatal dopamine and binding to the dopamine transporter (DAT), suggesting a loss of dopamine terminals. Because the loss of dopamine and DAT, however, do not necessarily reflect dopamine terminal degeneration, we have used silver staining and TH immunohistochemistry to further examine this issue. We have also examined the glial reaction using GFAP as a marker of astrocyte activation and OX-42 as a marker of activated microglia. Lastly, we have begun to explore the mechanism of synergy by investigating the role that the cytokine TNF-alpha might play in Tat + METH synergy. Our data indicate that the synergistic loss of dopamine is likely the result of dopamine terminal degeneration. This injury is not a direct result of the number of activated glia but does involve TNF-alpha.
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PMID:Human immunodeficiency virus-1 protein tat and methamphetamine interactions. 1710 16

A 20-year old man who had sex with men (MSM) presented with destructive osteomyelitis of the sternal bone and diffuse maculopapular rash. During laboratory evaluation he was found to have secondary syphilis and HIV with viral load of 28,000 copies per milliliter and CD4 count of 251 cells per microliter. Surgical debridement and biopsy of the sternal bone was performed. The biopsy examination demonstrated bone necrosis with perivascular infiltration of plasma cells and lymphocytes and rare hystiocytes. No granulomatous lesions were identified and acid-fast, fungal, silver, and Gram's stains did not show any organism. All cultures were negative. Real-time polymerase chain reaction (PCR) using probes targeting a pathogen-specific and highly conserved TpN47 gene of Treponema pallidum was performed on the DNA, extracted from the biopsy specimen and T. pallidum amplicons were detected. Patient was initially treated empirically with vancomycin, piperacillin/tazobactam and intravenous aqueous penicillin G. After confirming the diagnosis he completed 2 weeks of intravenous aqueous penicillin G treatment with resolution of osteomyelitis confirmed at follow-up visit after 6 weeks. Osteomyelitis is a rarely described manifestation of secondary syphilis. To the best of our knowledge, this is the first case of using T. pallidum DNA PCR to confirm the diagnosis of syphilitic osteitis. We suggest that osteomyelitis may be an underrecognized problem in patients with secondary syphilis, especially in HIV-coinfected individuals and PCR seems to be a valuable method in confirming the diagnosis.
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PMID:Destructive osteomyelitis associated with early secondary syphilis in an HIV-positive patient diagnosed by Treponema pallidum DNA polymerase chain reaction. 1746 16

Pneumocystis jiroveci (formerly carinii) pneumonia (PCP) is a serious opportunistic infection in children and adolescents with cancer. It was the most common cause of death among children receiving chemotherapy prior to the inclusion of PCP prophylaxis as part of standard care for children with leukemia. The incidence of PCP has decreased significantly since initiation of prophylaxis; however, breakthrough cases continue to occur. Hematologic malignancies, brain tumors necessitating prolonged corticosteroid therapy, hematopoietic stem cell transplantation, prolonged neutropenia, and lymphopenia are the most important risk factors for PCP in children not infected with HIV. Of children with leukemia, 15-20% may develop PCP in the absence of prophylaxis. Infection with P. jiroveci occurs early in life in most individuals. However, clinically apparent disease occurs almost exclusively in immunocompromised persons. Dyspnea, cough, hypoxia, and fever are the most common presenting symptoms of PCP. Chest radiography and high-resolution CT scans of the chest demonstrate a characteristic ground-glass pattern. Induced sputum analysis and bronchoalveolar lavage are the diagnostic procedures of choice. Gomori's methenamine-silver stain, Geimsa or Wright's stain, and monoclonal immunofluorescent antibody stains are most commonly used to make a diagnosis. However, identification of P. jiroveci DNA using polymerase chain reaction assays in bronchoalveolar lavage fluid is more sensitive. Trimethoprim-sulfamethoxazole (TMP-SMZ; cotrimoxazole) is the recommended drug for the treatment of PCP. Patients who are intolerant of TMP-SMZ or who have not responded to treatment after 5-7 days of therapy with TMP-SMZ should be treated with pentamidine. A short course of corticosteroids is recommended for moderate to severe cases of PCP within the first 72 hours after diagnosis. Mutations in the dihydropteroate synthetase gene may confer resistance to TMP-SMZ; however, the clinical relevance of these mutations is not well established. TMP-SMZ is the most commonly used agent for prophylaxis. Myelosuppression is the most important adverse effect of TMP-SMZ and the most frequent cause for choosing alternative prophylactic agents in children undergoing chemotherapy. Alternative agents for chemoprophylaxis include dapsone, aerosolized pentamidine, and atovaquone. Alternative prophylactic agents must be used in patients developing myelosuppression secondary to TMP-SMZ or dapsone.
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PMID:Management of Pneumocystis jiroveci pneumonia in children receiving chemotherapy. 1792 2

12B75, 274150; Abacavir sulfate/lamivudine, Abatacept, Ad2/HIF-1alpha, Adalimumab, Adefovir, Adefovir dipivoxil, AGN-201904-Z, AIDSVAX, Albinterferon alfa-2b, Alemtuzumab, Aliskiren fumarate, Alvimopan hydrate, Amlodipine besylate/atorvastatin calcium, Amlodipine besylate/Olmesartan medoxomil, Ammonium tetrathiomolybdate, Amodiaquine, Apaziquone, Aprepitant, Arsenic trioxide, Artesunate/Amodiaquine, Ascorbic acid, Atazanavir sulfate, Atazanavir/ritonavir, Atomoxetine hydrochloride, Atrigel-Leuprolide, Axitinib; Bevacizumab, Binodenoson, Bortezomib, Bovine lactoferrin; Calcipotriol/betamethasone dipropionate, Carisbamate, Certolizumab pegol, Ciclesonide, Conivaptan hydrochloride, CP-690550, CP-751871, Cypher; Dapivirine, Darbepoetin alfa, Darunavir, Dasatinib, del-1 Genemedicine, Denosumab, Desloratadine, Dexlansoprazole, DiabeCell, Drospirenone/ethinylestradiol, DTaP-HepB-IPV, Duloxetine hydrochloride, Dutasteride; Eculizumab, Eldecalcitol, Eletriptan, Emtricitabine, Entecavir, Eritoran tetrasodium, Ertapenem sodium, Escitalopram oxalate, Eslicarbazepine acetate, Esomeprazole magnesium, Estradiol acetate, Eszopiclone, ETEC vaccine, Etoricoxib, Exenatide, Ezetimibe; Fluticasone furoate, Fosmidomycin, Fosmidomycin/clindamycin; Glutamine; Heat Shock Protein 10, Hepatitis B hyperimmunoglobulin, HIV vaccine, Hochuekki-to, Human Albumin, Human papillomavirus vaccine; Immune globulin subcutaneous [human], IMP-321, Interferon omega, ISIS-301012, Istaroxime; Japanese encephalitis virus vaccine; Latanoprost/timolol maleate, Lenalidomide, Linaclotide acetate, Lumiracoxib, LY-517717; Malaria vaccine, MAS-063D, Meningitis B vaccine, Mepolizumab, Methylnaltrexone bromide, Micafungin sodium, MK-0822A, Morphine glucuronide, Morphine hydrochloride, Mycophenolic acid sodium salt; Natalizumab, Nesiritide, Norelgestromin/ethinyl estradiol, NT-201; Oblimersen sodium, Olmesartan medoxomil, Olmesartan medoxomil/hydrochlorothiazide, Omalizumab, Otamixaban; Paclitaxel nanoparticles, Panitumumab, Panobinostat, Parathyroid hormone (human recombinant), Parecoxib sodium, Pegfilgrastim, Peginterferon alfa-2a, Peginterferon alfa-2b, Pegvisomant, PI-88, Pimecrolimus, Pneumococcal 7-valent conjugate vaccine, Pneumococcal 9-valent conjugate vaccine, Pneumococcal conjugate vaccine, Poloxamer-188, Prasugrel, Pregabalin, Prulifloxacin; R-109339, Ramipril/amlodipine, Ranolazine, Rasburicase, rHA influenza vaccine, Ro-50-3821, Rosuvastatin calcium, Rotavirus vaccine, Rotigotine, Ruboxistaurin mesilate hydrate; Satavaptan, SC-75416, Solifenacin succinate, Sorafenib, Sugammadex sodium, Sunitinib malate, Synthetic conjugated estrogens B; Tadalafil, Talnetant, Taxus, Tegaserod maleate, Telbivudine, Temsirolimus, Tenofovir disoproxil fumarate, Tetomilast, Tiotropium bromide, Tipifarnib, Tofimilast, Tremelimumab, Trimethoprim; Udenafil, Urocortin 2; Valdecoxib, Vernakalant hydrochloride; XP-828L.
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PMID:Gateways to clinical trials. 1798 11

A 22-year-old man was admitted to our hospital with fever, cough and dyspnea. His chest radiograph showed diffuse ground-glass attenuation in both lung fields. Arterial blood gas analysis showed hypoxemia (PaO2 28.7 Torr breathing room air) and he required mechanical ventilation within 6 hours after admission. Gomori methenamine silver (GMS) stain of the bronchoalveolar lavage (BAL) fluid smear showed round and indented organisms, and polymerase chain reaction revealed pneumocystis jirovecii in the BAL fluid. The HIV antibody was positive and peripheral blood CD4-positive lymphocytes decreased to 4.0%. Pneumocystis pneumonia complicated with acquired immunodeficiency syndrome (AIDS) was diagnosed. There was no four-fold rise in screen viral titers. We treated him with antibiotics, trimethoprim-sulfamethoxazole, ganciclovir, fos-fluconazole, steroid pulse therapy and sivelestat sodium hydrate. Respiratory failure was relieved within 5 days following treatment. The percentage of neutrophils in the BAL fluid was elevated (44.6%). Neutrophil elastase on admission was increased and improved to the normal range after treatment. Sivelestat sodium hydrate is an anti-neutrophil elastase inhibitor and may be one of the treatment options for acute respiratory failure due to pneumocystis pneumonia in AIDS patients.
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PMID:[Acute respiratory failure due to pneumocystis pneumonia successfully treated with combined use of sivelestat sodium hydrate]. 1859 91


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