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Query: UMLS:C0001175 (AIDS)
 120,706 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cranial neuropathies were present in 5 patients with positive serology for the human immunodeficiency virus. Two patients presented with abnormalities of ocular movements (3rd, 4th), two with an isolated unilateral facial nerve palsy and one with a lesion of the accessory nerve. Neurological symptoms and signs are present in approximately 60 to 80 p. 100 of cases of the acquired immunodeficiency syndrome, but cranial neuropathies affect only 2 to 3 p. 100 of the patients. The isolation of the human immunodeficiency virus from the nerve suggest a direct role, but an indirect immune mechanism may also be present. Some of the patients with aseptic meningitis or subacute encephalopathy have demonstrated involvement of cranial nerves, mainly 2nd, 7th and 8th. Systemic tumors (lymphoma) may involve the central nervous system by diffuse meningeal invasion with lesions of 3rd, 4th and 6th nerves. Opportunist infections like Herpes zoster or Cytomegalovirus may produce cranial neuropathies (2nd, 5th). Isolated mononeuropathies or cranial nerves palsies have also been reported in patients treated with chemotherapeutic agents like vinca alkaloids.
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PMID:[Polyneuritis of cranial nerves and acquired immunodeficiency syndrome (AIDS): 5 cases]. 319 6

We examined 42 patients with the acquired immune deficiency syndrome: 11 of these had retinal lesions. In this study we reported five cases; all were examined within several weeks of admission to the Maggiore Hospital, and at various intervals thereafter. Ophthalmic evaluation included determination of visual acuity, slit-lamp examinations, direct ophthalmoscopy with the pupil dilated, fundus photography and fluorescein angiography. Peripheral blood mononuclear cells were isolated during gradient density centrifugation. Lymphocyte subsets were determined by immunofluorescence with monoclonal antibodies of the OKT series. All patients demonstrated a reduction of the ratio of T-helper to T-suppressor. Patient no. 1 was a 41 year-old hemophiliac man became ill (ARC) in June 1986; initially the patient had no ocular lesions. After five months developed bilateral retinal cotton wool spots. The patient's clinical conditions progressively worsened during the ensuing months and after fifteen months he felt a decreased vision in left eye: retinal examination disclosed a presumed CMV retinitis. Patient no. 2 was a 30 year-old intravenous drug-user man. At the time of the admission (AIDS) ophthalmologic evaluation revealed multiple cotton wool spots in both eyes. These changed of number and size during the following months. This patient was treated with ganciclovir (dihydroxy propoxymethyl guanine) because developed a CMV encephalopathy. We noted after this treatment a strong reduction of the cotton wool spots without an improvement of the general conditions and he died a month later. Patient no. 3 was a 26 year-old drug-user woman admitted for ARC. Ophthalmologic evaluation disclosed in right eye a presumed CMV retinitis with vascular sheathing and hemorrhages, and in left eye a little white retinal lesion (an initial retinitis) and cotton wool spots. The general and the retinal conditions rapidly worsened and she died three months later. Patient no. 4 was a 24 year-old women, intravenous drug-user, admitted for AIDS complicated by central nervous system infection by Toxoplasmic Gondii. Ocular examination revealed in right eye retinal cotton wool spots, and in left eye a white chorioretinal lesion with vitritis attributed to Toxoplasma Gondii. This retinochoroiditis improved after empiric therapy with sulfonamides and pyrimethamine. Patient no. 5 was a 37 year-old bisexual man admitted for AIDS. The findings on ophthalmologic examination were: CMV retinitis in right eye and retinal cotton wool spots in left eye. Treatment with ganciclovir resulted in an improvement of general symptoms.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Retinographic and angiographic study of ocular lesions detected in AIDS]. 320 13

Recombinant human colony-stimulating factor-1-treated human peripheral blood-derived monocytes-macrophages are efficient host cells for recovery of the human immunodeficiency virus (HIV) from blood leukocytes of patients with acquired immunodeficiency syndrome. These cells can be maintained as viable monolayers for intervals exceeding 3 months. Infection with HIV resulted in virus-induced cytopathic effects, accompanied by relatively high levels of released progeny virus, followed by a prolonged low-level release of virus from morphologically normal cells. In both acutely and chronically infected monocytes, viral particles were seen budding into and accumulating within cytoplasmic vacuoles. The number of intravacuolar virions far exceeded those associated with the plasma membrane, especially in the chronic phase, and were concentrated in the perinuclear Golgi zone. In many instances, the vacuoles were identified as Golgi elements. Fusion of virus-laden vacuoles with primary lysosomes were rare. The pattern of cytoplasmic assembly of virus was observed with both HIV types 1 and 2 and in brain macrophages of an individual with acquired immunodeficiency syndrome encephalopathy. Immunoglobulin-coated gold beads added to acutely infected cultures were segregated from the vacuoles containing virus; relatively few beads and viral particles colocalized. The assembly of HIV virions within vacuoles of macrophages is in contrast to the exclusive surface assembly of HIV by T lymphocytes. Intracytoplasmic virus hidden from immune surveillance in monocytes-macrophages may explain, in part, the persistence of HIV in the infected human host.
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PMID:Cytoplasmic assembly and accumulation of human immunodeficiency virus types 1 and 2 in recombinant human colony-stimulating factor-1-treated human monocytes: an ultrastructural study. 326 Jun 31

A 22-year-old man who underwent syngeneic bone marrow transplantation (BMT) for acute lymphoblastic leukemia acquired a human immunodeficiency virus (HIV) infection by transfusion of blood products from a donor at risk. The manifestations were acute encephalopathy together with immune thrombocytopenia in the early posttransplant period, and acquired immunodeficiency syndrome (AIDS) developed 20 months after BMT. Because he had a syngeneic donor, the possibility of reconstituting the immune system was investigated by repeated transfer of healthy syngeneic lymphocytes and by combining repeated transfer of syngeneic lymphocytes with the antiviral agent suramin to protect the infused leukocytes from being attacked by HIV. No improvement was observed clinically or in the patient's immune functions by these efforts.
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PMID:Syngeneic leukocytes together with suramin failed to improve immunodeficiency in a case of transfusion-associated AIDS after syngeneic bone marrow transplantation. 327 51

Human immunodeficiency virus type 1 (HIV-1) has been clearly associated with a variety of new illnesses, including profound immunodeficiency (acquired immune deficiency syndrome [AIDS]), wasting syndromes (formerly termed AIDS-related complex [ARC]) and neurologic syndromes, including neuropathy, myelopathy and encephalopathy (often termed subacute encephalitis or AIDS dementia complex). HIV-1 preferentially infects T lymphocytes by binding to a membrane receptor protein, CD4, associated with helper function. The virus can also attack macrophages and, possibly, other cells such as neuronal cells, colonic epithelial cells and B lymphocytes. Infection of macrophages or monocytes may be involved in neurologic disease. Knowledge about HIV-1 has rapidly increased, and investigators have characterized its structure, ways in which it infects cells, replicates and is cytopathic for certain cells, and how the immune system responds to it. The ideal vaccine would prevent adsorption of the virus into the cell, but it is difficult to develop stable resistance because the virus has many antigenic patterns and mutates frequently. The results of vaccine trials in animals have not been promising, but work is being done with monoclonal antibodies. Antiviral therapies being investigated include those to prevent virus binding and entry, to inhibit reverse transcription, to inhibit the virus's life cycle and to restore immune competence in immunocompromised patients.
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PMID:Vaccine and antiviral strategies against infections caused by human immunodeficiency virus. 328 28

AIDS, presumably caused by the human retrovirus, human immunodeficiency virus (HIV), is a disease with multiple pathologies, most of which are the consequence of a profound immunodeficiency. The first two sections of this review focus primarily on the normal development and function of the cells of the immune system and the known abnormalities that occur in this system in AIDS patients. Very little is known of the pathogenesis, in humans, of the four major clinical manifestations of AIDS--immunodeficiency, encephalopathy, Kaposi's sarcoma, and lymphoma. Because most pathologic studies derive from autopsy findings in terminal AIDS patients, it has been difficult to track the course of HIV infection from the time of initial contact with the virus through the evolution of the disease. Therefore, the final section of this review focuses on actual and potential animal models of AIDS and how such models might be valuable for studies on the pathogenesis of the disease, the development of relevant vaccines, and the testing of potential therapies.
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PMID:Approaches to an understanding of pathogenetic mechanisms in AIDS. 328 66

In an autopsied case of a 37-year-old man with acquired immune deficiency syndrome (AIDS), multinucleated giant cell encephalopathy was noted in close proximity to multiple nodules of primary lymphoma of the brain. Some multinucleated giant cells and macrophages contained HTLV-III-like viral particles. Nuclear bridges, thin strands connecting individual nuclei with one another, were observed with both light and electron microscopes within some of the multinucleated giant cells. There were also thin tapering nuclear processes, which were probably part of nuclear bridges. The possibility that the nuclear bridges and processes represent amitotic nuclear division is discussed.
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PMID:Nuclear bridges in multinucleated giant cells associated with primary lymphoma of the brain in acquired immune deficiency syndrome (AIDS). 343 11

In addition to central nervous system (CNS) opportunistic infections and neoplasms, patients with acquired immunodeficiency syndrome (AIDS) develop unexplained dementia and encephalopathy and degeneration of the white matter. We studied autopsied brains from 20 adult patients who expired from AIDS to determine the relationship of human immunodeficiency virus (HIV) infection to white matter lesions and to clinical findings. In four patients with dementia/encephalopathy and abnormalities of the white matter, there was evidence of HIV infection as shown by in situ hybridization. In contrast, the remaining 16 patients who had no evidence of white matter degeneration revealed no hybridization to the HIV probe. The cells infected with HIV included endothelial cells, perivascular macrophages/monocytes, and multinucleated giant cells and were found in or adjacent to white matter degeneration. These results demonstrate a correlation between HIV-infected cells and AIDS leukoencephalopathy and provide further evidence for HIV-related dementia/encephalopathy.
AIDS Res Hum Retroviruses 1987
PMID:Human immunodeficiency virus (HIV) infection in brains with AIDS-related leukoencephalopathy. 344 27

The retrovirus that causes acquired immune deficiency syndrome (AIDS) is now designated the human immunodeficiency virus (HIV). The cerebrospinal fluid (CSF) of 27 children with HIV infection was assayed for intra-blood-brain barrier (IBBB) synthesis of HIV-specific antibodies and for the presence of HIV antigen. In this cohort, 11 children had a progressive encephalopathy (PE), 9 had a static encephalopathy (SE), and 7 had normal neurological findings (N). IBBB synthesis of HIV-specific antibodies was identified (using matched serum and CSF specimens) in 7 of 11 children with PE, 4 of 9 children with SE, and 2 of 7 children with N. HIV antigen was found (using a highly sensitive solid-phase enzyme immunoassay) in the CSF of 8 of 11 children with PE, none of the children with SE, and none of the 7 children with N. On the basis of these data, we conclude that: IBBB synthesis of HIV antibodies indicates invasion of the central nervous system but may reflect prior or current infection; and HIV antigen in CSF indicates viral expression and correlates with the occurrence of PE. These findings strongly implicate HIV as the causative agent of PE in these children. The assay for HIV antigen in the CSF may be of value in determining the prognosis of children with HIV infection and for evaluating the efficacy of therapeutic agents against this retrovirus.
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PMID:Expression of human immunodeficiency virus in cerebrospinal fluid of children with progressive encephalopathy. 347 86

The presence of human immunodeficiency virus (HIV) antigens in cerebrospinal fluid (CSF) was associated with progressive encephalopathy in adult and pediatric patients with acquired immunodeficiency syndrome (AIDS). HIV antigen was detected in CSF from 6 of 7 AIDS patients with progressive encephalopathy. By contrast, HIV antigen, whether free or complexed, was detected in CSF from only 1 of 18 HIV antibody seropositive patients without progressive encephalopathy and from 0 of 8 experimentally infected chimpanzees without clinical signs. Intra-blood-brain barrier synthesis of HIV-specific antibody was demonstrated in the majority of patients with AIDS (9/12) or at risk for AIDS (8/13) as well as in the experimentally infected chimpanzees, indicating HIV-specific B-cell reactivity in the brain without apparent neurological signs. In 6 of 11 patients with HIV infection, antibodies synthesized in the central nervous system were directed against HIV envelope proteins. Active viral expression appears to be necessary for both the immunodeficiency and progressive encephalopathy associated with HIV infection.
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PMID:Intra-blood-brain barrier synthesis of human immunodeficiency virus antigen and antibody in humans and chimpanzees. 347 87


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