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1/14. Immunocytochemical characterization of cytomegalovirus (CMV) infected giant cells in perinatal acquired human immunodeficiency virus (hiv) infection.

    In a pediatric case of necrotizing CMV myelitis after perinatal hiv infection characteristic cytomegalic cells, which could not be attached to a particular cell line by cell morphology, were studied after immunostaining with monoclonal and polyclonal antibodies raised against GFAP, S100 protein, NSE, synaptophysin, factor viii, vimentin, macrophages, leukocytes, CMV, HSV I II, toxoplasma, and hiv 1 gp41. astrocytes, oligodendrocytes, neurons, ependymal and endothelial cells, macrophages, and schwann cells stained positively with CMV antiserum. With regard to their immunological features the majority of cytomegalic cells ("owl eye cells") was identified as astrocytes, and in decreasing frequency, the remainder was characterized as macrophages, mesenchymal, and endothelial cells. It is concluded that CMV giant cells represent one phase of virus induced cell transformation, not only one single, but numerous cell types are exposed to after CMV infection.
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2/14. Unusual development of polyoma virus in the brains of two patients with the acquired immune deficiency syndrome (AIDS).

    Two hiv-positive male patients presented with a variety of symptoms including hemiparesis, unsteadiness, progressive loss of vision and poor memory. There were multiple non-enhancing lesions shown by CT scan in the white matter of the cerebral hemispheres. Specimens obtained by burr-hole biopsy showed the features of progressive multifocal leucoencephalopathy (PML) in both cases. Electron microscopy demonstrated round and rod shaped particles of papovavirus in the nuclei and cytoplasm of oligodendrocytes and in processes of astrocytes where abnormal and florid modes of viral replication were seen. Additional features observed were viral particles suggestive of an enterovirus in Case 1 and, in both specimens, massive membrane proliferation within both nuclei and cytoplasm of infected cells together with the presence of tubuloreticular structures (TRS) in the cytoplasm of endothelial cells. At post-mortem, the brain of patient 2 showed PML and hiv encephalitis. The presence of hiv was confirmed by immunohistochemical methods. We suggest that in AIDS patients the abnormality of the immune system induced by hiv causes abnormal replication patterns of papovavirus in the brain. In addition, these cases confirm the frequent occurrence in AIDS patients of TRS, now considered to be a marker for hiv.
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3/14. The fine structure of acquired immunodeficiency syndrome encephalopathy.

    Involvement of the central nervous system with the human immunodeficiency virus is thought to underlie the clinical and pathologic features of acquired immunodeficiency syndrome (AIDS) encephalopathy. Although morphologic, immunocytochemical, and molecular data point to predominant human immunodeficiency virus infection of multinucleated and mononuclear macrophages, neuroglial and other cells are thought to be involved as well. Electron microscopic studies of biopsy tissue that might further define the neuropathologic changes have been limited. The opportunity to study well-preserved biopsy tissue from a 38-year-old man with the acute onset of dementia and AIDS encephalopathy prompted this report. Human immunodeficiency virus was seen budding from the surface of multinucleated and mononuclear cells with morphologic features of macrophages; a rare astrocyte process showed evidence of viral infection as well. macrophages were noted within the walls of blood vessels and in intimate contact with lymphocytes within the neuropil. Notably rare were tubuloreticular inclusions, interferon-related cytoplasmic structures commonly found in systemic endothelial cells and lymphocytes in AIDS. Their relative scarcity may signify reduced interferon production in AIDS encephalopathy.
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4/14. Massive neuronal destruction in human immunodeficiency virus (hiv) encephalitis. A clinico-pathological study of a pediatric case.

    Human immunodeficiency virus (hiv) encephalitis in children with AIDS includes a diffuse white matter disease associated with an inflammatory cell infiltrate that features multinucleated giant cells. cerebral cortex is relatively preserved and only focal loss of purkinje cells in the cerebellum has been observed. We describe a case of encephalitis in a child with AIDS in which there was massive and diffuse destruction of the cerebral cortex with severe neuronal loss, marked inflammatory perivascular infiltrate with abundant multinucleated cells and large pleomorphic reactive astrocytes. Similar findings were present in the basal ganglia. Moreover, the cerebellum disclosed a complete loss of Purkinje and granule cells. These findings could not be related to an ischemic mechanism or to an associated opportunistic infection. Electron microscopy showed numerous hiv particles. This case illustrates a different pattern of CNS involvement by hiv and emphasizes the destructive capacity of this neurotropic virus for neural tissue.
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5/14. Human immunodeficiency virus and papovavirus infections in acquired immunodeficiency syndrome: an ultrastructural study of three cases.

    A wide variety of neurologic conditions associated with the acquired immunodeficiency syndrome (AIDS) have been attributed to human immunodeficiency virus (hiv) infection of the central nervous system (CNS). Tissue samples from the brains of three patients with AIDS, diagnosed as having CNS toxoplasmosis on the basis of computed tomographic scans of the head, were studied by transmission electron microscopy. In two, hiv particles were observed budding from, in close association with, and in cytoplasmic vacuoles of mononuclear and multinucleated macrophages, but no other cell types. The patient with the greatest number of hiv particles also had large amounts of papovavirus (progressive multifocal leukoencephalopathy) in the nuclei of oligodendroglial cells and in the cytoplasm of astrocytes. These astrocytes often had atypical features at the light microscopic level. Following an initial biopsy that showed only hiv, primary CNS lymphoma was diagnosed by needle biopsy and confirmed at autopsy in a second case. A diagnosis of progressive multifocal leukoencephalopathy was rendered by transmission electron microscopy in a third case, but no hiv was detected. toxoplasmosis was not confirmed in any of the three cases. diagnosis of CNS lesions in patients with AIDS should not rely exclusively on radiography but include biopsy for both light and transmission electron microscopy. Transmission electron microscopy can be employed to reveal hiv and papovavirus infections not discernible at the light microscopic level and should be used as a diagnostic tool in hiv-related infections.
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6/14. Human T-cell lymphotropic virus type III infection of the central nervous system. A preliminary in situ analysis.

    patients with the acquired immunodeficiency syndrome (AIDS) are subject to a spectrum of central nervous system (CNS) disorders. Recent evidence implicates the human T-cell lymphotropic virus type III (HTLV-III) in the pathogenesis of some of these illnesses, although, the cells infected by the virus have yet to be identified. Using in situ hybridization, we examined brain tissue from two patients with AIDS encephalopathy for the presence of HTLV-III rna. In both cases, viral rna was detected and concentrated in, though not limited to, the white matter. The CNS cells most frequently infected included macrophages, pleomorphic microglia, and multinucleated giant cells. Less frequently, cells morphologically consistent with astrocytes, oligodendroglia, and rarely neurons were also infected. The findings strengthen the association of HTLV-III with the pathogenesis of AIDS encephalopathy. in situ hybridization can be applied to routinely prepared biopsy tissue in the diagnosis of HTLV-III infection of the CNS.
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7/14. Progressive encephalitis three months after resolution of cutaneous zoster in a patient with AIDS.

    A 37-year-old homosexual man with the acquired immune deficiency syndrome (AIDS) developed progressive, ultimately fatal, neurological deficits 12 weeks after a course of cutaneous zoster. Premortem radiological procedures and cerebrospinal fluid analyses were nondiagnostic. At postmortem examination, several opportunistic infections associated with AIDS were recognized. Throughout the brain, necrotic and demyelinative lesions were present, suggestive of progressive multifocal leukoencephalopathy. However, light microscopical examination showed numerous Cowdry type A intranuclear inclusions in astrocytes, oligodendrocytes, and neurons near the periphery of the lesions. herpes zoster encephalomyelitis was diagnosed and confirmed by electron microscopy, peroxidase-antiperoxidase staining, and by Southern blot analysis of dna extracted from brain tissue. This case provides insight into the pathogenesis of zoster-associated encephalomyelitis and suggests another agent to be considered in the differential diagnosis of encephalopathy in patients with AIDS and other disorders of immunological impairment.
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8/14. HTLV-III/LAV-like retrovirus particles in the brains of patients with AIDS encephalopathy.

    It has been postulated that the retrovirus HTLV-III/LAV thought to be the etiologic agent of AIDS also infects the central nervous system and directly causes AIDS encephalopathy. Electron microscopical studies performed on brain sections from three patients with AIDS complicated by progressive encephalopathy revealed structures morphologically consistent with HTLV-III/LAV retrovirus particles. The particles were located principally within multinucleated giant cells but were also present in astrocytes. Many particles were also noted in the extracellular space.
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9/14. brain stem encephalitis due to varicella-zoster virus in a patient with AIDS.

    We describe a patient infected with human immunodeficiency virus (hiv) who had localized brain stem encephalitis due to varicella-zoster virus (VZV) and no cutaneous eruption. diagnosis of the infection was based on the presence of Cowdry type A intranuclear inclusions in neurons, astrocytes, and oligodendrocytes positive for VZV (as shown by immunochemical staining). Although this infection is rare, we demonstrate the need for clinicians to include VZV infection in the differential diagnosis of rapidly progressive multiple cranial nerve palsies in hiv-infected patients, particularly because specific treatment for VZV infection is effective and relatively safe.
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10/14. Concurrent herpes simplex type 1 necrotizing encephalitis, cytomegalovirus ventriculoencephalitis and cerebral lymphoma in an AIDS patient.

    Unlike cytomegalovirus (CMV) ventriculoencephalitis, herpes simplex virus type 1 necrotizing encephalitis has only rarely been observed in AIDS patients. A 40-year-old bisexual man was followed for an HIV1 infection from 1987 onwards. In June 1993 he was referred for sudden confusion, left hemiparesia and fever. The blood contained less than 10 CD4 lymphocytes/mm3. The patient remained comatose and febrile, and died 4 weeks later. In coronal sections of the brain there was necrosis of the internal parts of the left temporal lobe, necrosis of certain areas of the ventricular walls and a small tumor at the top of the right frontal lobe, which proved to be a polymorphic high-grade lymphoma. CMV ventriculoencephalitis lesions were prominent in the ventricular walls of the occipital lobes and there was a strong nuclear signal for CMV using in situ hybridization. herpes simplex virus type 1 was shown in the nuclei and cytoplasm of certain neurons and astrocytes in the borders of the necrotized temporal lobe areas by immunohistochemistry, in situ hybridization and electron microscopy, whereas in situ hybridization and immunohistochemistry for CMV were negative in such areas. Necrotizing type 1 encephalitis must not be overlooked in immunodeficient patients.
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