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

Early HIV-1 invasion of the central nervous system has been demonstrated by many cerebrospinal fluid studies; however, most HIV-1 carriers remain neurologically unimpaired during the so called "asymptomatic" period lasting from seroconversion to symptomatic AIDS. Therefore, neuropathological studies in the early pre-AIDS stages are very few, and the natural history of central nervous system changes in HIV-1 infection remains poorly understood. Examination of brains of asymptomatic HIV-1 positive individuals who died accidentally and of rare cases with acute fatal encephalopathy revealing HIV infection, and comparison with experimental simian immunodeficiency virus and feline immunodeficiency virus infections suggest that, invasion of the CNS by HIV-1 occurs at the time of primary infection and induces an immunological process in the central nervous system. This includes an inflammatory T-cell reaction with vasculitis and leptomeningitis, and immune activation of brain parenchyma with increased number of microglial cells, upregulation of major histocompatibility complex class II antigens and local production of cytokines. Myelin pallor and gliosis of the white matter are usually found and are likely to be the consequence of opening of the blood brain barrier due to vasculitis; direct damage to oligodendrocytes by cytokines may also interfere. These white matter changes may explain, at least partly, the early cerebral atrophy observed, by magnetic resonance imaging, in asymptomatic HIV-1 carriers. In contrast, cortical damage seems to be a late event in the course of HIV-1 infection. There is no significant neuronal loss at the early stages of the disease, no accompanying increase in glial fibrillary acid protein staining in the cortex, and only exceptional neuronal apoptosis. Although HIV-1 proviral DNA may be demonstrated in a number of brains, viral replication remains very low during the asymptomatic stage of HIV-1 infection. This makes it likely that, although opening of the blood brain barrier may facilitate viral entry into the brain, specific immune responses including both neutralising antibodies and cytotoxic T-lymphocytes, continuously inhibits viral replication at that stage.
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PMID:Neuropathology of early HIV-1 infection. 886 43

The FIV (feline immunodeficiency virus) induces in cats brain changes presenting similarities with those observed in human immunodeficiency virus infection. This FIV model was used to study the relationship between viral load in brain, in lymphoid organs and central nervous system (CNS) changes during the early and late stages of infection. Early brain changes were analyzed in animals experimentally infected with two different FIV isolates and sacrificed at 7 and 15 days, 1, 2, 6, and 12 months post inoculation (p.i.). Late CNS abnormalities were analyzed in naturally FIV-infected cats referred to the Veterinary School of Nantes. For each animal, one cerebral hemisphere was fixed and examined using routine techniques. The characterization of FIV replicating cells by in situ hybridization was performed on the other half frozen hemisphere on sections performed in the anterior and the median regions of the brain. During the early stages of infection, moderate gliosis with glial nodules and sometimes white matter pallor and meningitis were associated with few infected cells scattered in the brain. Infection was an early event as infected cells could be detected in brain at 7 p.i. For each cat, these findings were found identical in the two analyzed areas. During the late stages, brain lesions and the number of virus replicating cells increased especially in animals with perivascular infiltrates. The multinucleated giant cells encephalitis was never observed and the number of FIV replicating cells scattered in the whole brain was always low. This discrepancy between the number of replicating cells and the brain lesions, corroborates the hypotheses suggesting that brain injuries may be mediated via diffusive factors and amplification processes through cytokine cascades and cell activations.
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PMID:Virus load and neuropathology in the FIV model. 897 19

The case of a 25-year-old male agricultural laborer with HIV infection and Pneumocystis carinii pneumonia (PCP) is described, whose radiological lesions simulated pulmonary tuberculosis. He presented with loss of weight and appetite of 6 months' duration, cough with expectoration and minimal hemoptysis for 2 months, chest pain, diarrhea with fever, and odonophasia for 1 month. He had received antitubercular treatment (rifampicin 450 mg and isoniazid 300 mg) 2 months prior to admission. He had been promiscuous, having had multiple sexual contacts with prostitutes. General examination demonstrated marked emaciation, pallor, dyspnea, and oral candidiasis. Auscultation indicated fine medium pitched crackles in both infraclavicular regions. Blood for ELISA and immunocomb test were positive for HIV-1 antibodies. Hemogram revealed Hb 6 gm%, and TLC with polymorphs 63%, lymphocytes 30%, eosinophils 5%, and basophils 2%. The total lymphocyte count was 2100/cu. mm. Chest roentgenography revealed bilateral diffuse homogenous infiltrative lesions involving both lungs, with evidence of multiple bilateral cavitation. Therapy included antitubercular treatment with ethambutol, isoniazid, rifampicin, and pyrazinamide, along with Gentian violet mouth paint and ketoconazole orally, 200 mg bid. The patient developed progressive respiratory distress and died on the 7th day after admission. Limited autopsy of both lungs showed foamy eosinophilic material filling the alveolar space, and Grocett's methenamine silver staining showed cyst walls of P. carinii as black. There was no evidence of pulmonary tuberculosis. In the present case, the diagnosis of PCP should have been kept in mind to increase median survival time (25.9 vs. 12.6 months without treatment) with the treatment of choice of trimethoprim plus sulphamethoxizole in doses of 20 and 100 mg/kg/day. Early diagnosis and treatment will improve the mean survival time in cases of PCP with HIV infection.
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PMID:Pneumocystis carinii pneumonia simulating as pulmonary tuberculosis in AIDS. 901 80

We have examined brain sections from 55 autopsy cases of AIDS for the prevalence and severity of axonal damage, assessed using beta-amyloid precursor protein (beta APP) immunoreactivity as a marker of such damage. The cases were subdivided into cases with HIV encephalitis with multinucleated giant cells (MGC), cases with other specific pathology, such as cerebral toxoplasmosis or lymphoma, cases with non-specific pathology and cases with no pathology. Significantly more foci containing beta APP+ axons were found in cases with HIV encephalitis with MGC (80%) and in cases with other specific pathology (58%) than in those with non-specific (30%) or no pathology (30%). The prevalence and abundance of beta APP+ axons generally paralleled the severity of pallor of myelin staining of cerebral white matter in cases without other specific pathology but in 4 cases without any pallor of myelin staining beta APP+ axons were present, suggesting that it may be a more sensitive marker of some forms of white matter damage in HIV infection than myelin pallor. Foci of beta APP+ axons were found in subcortical and deep white matter but did not convincingly co-localise with foci of demonstrable HIV infection as indicated by the presence of MGC and HIV p24 immunoreactivity. In contrast, they showed an approximately perivascular distribution at some sites in all of the disease categories studied. We consider this localisation to be more suggestive of a vascular pathogenetic mechanism of deep white matter damage in HIV infection than a mechanism dependent on diffusion of local myelinotoxic products from foci of cerebral HIV infection.
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PMID:Cerebral white matter damage in HIV infection demonstrated using beta-amyloid precursor protein immunoreactivity. 903 67

Progressive disseminated histoplasmosis (PDH), a recognized defining illness of AIDS, is an opportunistic fungal infection caused by Histoplasma capsulatum. The authors report a case of PDH in a HIV-infected African child from a Histoplasma capsulatum non-endemic area. An 8-year-old girl from Kwazulu/Natal, South Africa, was admitted to King Edward VIII hospital with pyrexia and respiratory distress. Pale with generalized lymphadenopathy, she had been sick with general malaise and fever for 3 weeks. A punched-out painless ulcer was present on the child's lower left leg and she had ulcerative lesions on the tip of her tongue and the angle of her mouth. There was a tender hepatomegaly and clinical signs of pneumonia, while a chest roentgenogram showed right upper lobe consolidation with early cavitation. The purified protein derivative tuberculin skin test was negative and no acid-fast bacilli were detected on three sputum samples taken on different days. A Western blot test conducted for antibodies to HIV was positive. Additional laboratory tests were conducted. The patient was treated with parenteral acyclovir for herpesvirus infection, ceftriaxone for severe community-acquired pneumonia, and trimethoprim-sulfamethoxazole because Pneumocystis carinii infection was part of the clinical differential diagnosis. Bone marrow aspirate and trephine biopsy revealed yeast forms of H. capsulatum. The girl died on the second day of hospital admission, before antifungal therapy could be commenced.
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PMID:Disseminated histoplasmosis in a human immunodeficiency virus-infected African child. 910 50

In many patients with AIDS, severe neurologic deficits develop that have been designated the cf2HIV-associated cognitive-motor complex. cf1 Pathologically, these symptoms correlate with a low-grade inflammatory condition, referred to as cf2HIV encephalitis,cf1 in which the most characteristic change is the presence of multinucleated giant cells. Cortical changes include neuronal loss and alterations of dendrites and synapses. There is pallor of white matter generally associated with the mononuclear inflammatory infiltrates. The only cells that seem to be directly infected by HIV are the microglia/monocyte and the giant cells derived from fusion of monocytes. It is hypothesized, therefore, that cortical and white matter alterations in patients with this syndrome depend on the production of injurious soluble factors liberated by these cells and by astrocytes under the influence of many of these same factors. This article reviews recent advances in the understanding of these secondary effects and discusses pathogenetic mechanisms of tissue injury.
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PMID:Mechanisms of HIV infection of the central nervous system and pathogenesis of AIDS-dementia complex. 911 88

In the past, little attention has been given in the imaging literature to spinal cord findings in the human immunodeficiency syndrome. This article summarizes the major pathologic conditions found in the spinal cord in patients with AIDS and compares them to MR features. The details of toxoplasma myelitis, spinal cord lymphoma, HIV myelitis, and tract pallor are demonstrated. A review of literature and a description of the pathologic cord changes will help the reader understand the alterations of the spinal cord in patients with AIDS.
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PMID:Spinal cord lesions in patients with AIDS. 911 95

The pathogenesis of HIV-associated cognitive changes is poorly understood. Cytokines such as tumor necrosis factor-alpha (TNF-alpha) have been postulated to contribute to the mechanism of the neurological complications of HIV infection. One of the effects of TNF-alpha is to induce astrocyte proliferation in vitro. The purpose of this study was to look for a correlation between the expression of TNF-alpha, astrogliosis and the degree of cognitive impairment in 12 prospectively assessed AIDS cases without focal brain lesion, 8 of whom were demented. They were compared with 6 control patients without neurological disease. Neuropathological examination showed myelin pallor in 5 of the 8 demented patients. TNF-alpha expression was detected by immunohistochemistry in the midfrontal cortex, subcortical and deep white matter, and basal ganglia. Not only perivascular macrophages but also some microglial and endothelial cells were labeled. Most TNF-alpha-positive cells were in close contact with glial fibrillary acidic protein-positive astrocytes. They were more numerous than gp41-positive cells. Their density increased with increasing cognitive impairment and in parallel to the astrogliosis in the frontal cortex, basal ganglia and deep white matter. These findings further support the hypotheses that lesions of the deep white matter, driven by TNF-alpha, are associated with cognitive alteration, and that indirect effects of HIV infection in the brain participate in the development of HIV-associated dementia through a diffuse immune activation, mediated by cytokines.
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PMID:Tumor necrosis factor-alpha, microglia and astrocytes in AIDS dementia complex. 914 90

Half of AIDS dementia cases are associated with HIV-encephalitis or myelin pallor. Another half die with no HIV-related neuropathological changes. Previous observations suggest that cerebral dysfunction may result from more subtle cellular interactions. and that some of them may be mediated by cell adhesion molecules. In the present study the expression by astrocytes and endothelial cells of intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) was analysed as a function of the neuropathological diagnosis, the density of astrogliosis and of HIV-1 positive cells, and of the mental status. Twelve AIDS cases, without focal brain lesion, eight of whom were demented, were selected from a prospective study. They were compared with six control cases with multiple sclerosis, and with six control patients without neurological disease. ICAM-1 and VCAM-1 expression was localized by immunofluorescence and confocal microscopy. HIV protein gp41 was detected by immunohistochemistry on adjacent sections. Endothelial expression of ICAM-1 and VCAM-1 was significantly up-regulated in all AIDS patients. VCAM-1 only was related to myelin pallor. The density of VCAM-1 or ICAM-1 positive astrocytes increased in demented AIDS patients, independently of the neuropathological findings or the density of gp41 positive cells. Expression of cell adhesion molecules, together with other secondary mechanisms such as secretion of cytokines may play a role in the pathogenesis of white matter lesions leading to HIV-1-associated cognitive changes.
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PMID:Astrocytic adhesion molecules are increased in HIV-1-associated cognitive/motor complex. 916 Aug 93

Image texture analysis is used in a wide variety of applications in medical research. Neurovirulent simian immunodeficiency virus (SIV) infection in monkeys is considered a good model for HIV-1 infection in humans and causes neuropathological changes in white matter which can include diffuse myelin pallor, subtle white matter astrocytosis, perivascular macrophage infiltrates, and microglial nodules with multinucleated giant cells. The ability of image texture analysis to quantify these changes was evaluated. Sections of thionin-stained brain tissue from eight male rhesus macaques ranging in age from 42-59 months were used. Four animals served as controls and four animals were infected with neurovirulent SIVmac239/17E-R71 by bone marrow inoculation. Images of cerebral white matter were captured and analyzed by calculating 13 textural features based on statistical analysis of spatial co-occurrence matrices. Statistical analysis of the results included multiple comparisons using the Newman-Keuls multiple range test. The effect of variation in background illumination used at image acquisition was also evaluated. Ten of the 13 textural features used in this study successfully discriminated between tissue from control and SIV-infected animals and were consistent with independent neuropathological assessment. Three textural features were highly sensitive to variation in background illumination and found not useful in this application.
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PMID:Texture analysis of cerebral white matter in SIV-infected macaque monkeys. 921 May 75


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