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1/23. Virus-cell interaction in oligodendroglia, astroglia and phagocyte in progressive multifocal leukoencephalopathy. An electron microscopic study.

    A 46-year-old female, with an 11 year history of malignant lymphoreticular disease, developed a neurological illness clinically manifested by a focal mass lesion in the left frontal lobe. In biopsied tissue, immunofluorescence study revealed the presence of JC antigen in the glial cells. Histologically, the lesion was characteristic of PML consisting of PML consisting of focal necrosis in the subcortical white matter, numerous fat laden macrophages and marked hypertrophy of oligodendrocytes and astrocytes. By electron microscopy, hypertrophic astrocytes contained intranuclear viral particles consistent with papova virions and aggregates of intracytoplasmic viral particles consisting of a single to several virions tightly surrounded by a single membrane. The membrane appeared to have been derived from that of the cellular vesicles. Fusion of the virus-associated membrane to the astroglial plasmalemma occurred when the virions appeared to shift towards extracellular space. The virioncontaining astrocytes showed cytoplasmic "fibrillar hypertrophy" similar to the characteristic gigantic astroglias of PML. This fact would provide an additional evidence that these gigantic cells, although lacking identifiable viral structures, were the result of anaplastic transformation by jc virus. Many virus-bearing astroglias were noted to be in the early stage of cellular necrosis, of "edematous degeneration". This further indicates that the jc virus is capable of inducing both lytic and abortive astroglial infections. Many oligodendroglias were hypertrophic due to the presence of intranuclear viral particles and markedly increased numbers of microtubules and free ribosomes in the cytoplasm. Membrane-bound intracytoplasmic viral particles were also noted in the oligodendroglias. Some fat laden macrophages contained large intracytoplasmic viral bodies, presumably originating from phagocytized virus-bearing cells.
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2/23. Progressive multifocal leukoencephalopathy after autologous bone marrow transplantation and alpha-interferon immunotherapy.

    A patient with a stage IV mantle cell lymphoma (according to the REAL classification) was treated with high-dose chemotherapy and autologous bone marrow transplantation. One year later while on alpha-interferon immunotherapy she suffered from progressive loss of short-term memory and reported difficulties in recognizing objects. magnetic resonance imaging (MRI) showed a vast ring-enhancing lesion of the left postcentral parietal area. Serial stereotactic biopsies disclosed progressive multifocal leukoencephalopathy without JC-virus in the cerebrospinal fluid. Therapy with subcutaneous interleukin-2 (IL-2) every other day and intrathecal cytarabine once a week was started. After 4 weeks the patient refused further treatment. Nevertheless her condition improved over the next 8 months and MRI scans showed a marked improvement in the lesions.
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keywords = bone
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3/23. Progressive multifocal leucoencephalopathy with peripheral demyelinating neuropathy after autologous bone marrow transplantation for acute myeloblastic leukemia (FAB5).

    Progressive multifocal leucoencephalopathy is an opportunistic jc virus-related pathology occurring in immunocompromised patients. We report a case of severe cellular immunodeficiency in a patient who underwent autologous bone marrow transplantation for acute myeloblastic leukemia, and who subsequently developed progressive multifocal leucoencephalopathy, an unusual pathology in this context. Progressive multifocal leucoencephalopathy was preceded by a peripheral demyelinating neuropathy. We discuss the possible link between these two neuropathies, the possible aggravation or activation from CMV infection, as well as the possible contribution of bone marrow purging in the resultant cellular immunodeficiency.
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4/23. Macrophage association of polyomavirus in progressive multifocal leukoencephalopathy: an immunohistochemical and ultrastructural study. Case report.

    Progressive multifocal leukoencephalopathy (PML) in a patient following autologous bone marrow transplantation for a non-Hodgkin's centroblastic lymphoma was studied by immunohistochemistry and transmission electron microscopy. Our observations indicate that a large amount of polyomavirus, most probably jc virus, is taken up and segregated within vacuoles of macrophages by phagocytosis. A relevant role of macrophages in the pathogenesis of PML is emphasized.
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5/23. Comparison of PCR-amplified jc virus control region sequences from multiple brain regions in PML.

    The authors report a 14-year-old boy with wiskott-aldrich syndrome complicated by progressive multifocal leukoencephalopathy after allogeneic bone marrow transplantation. Several therapeutic approaches were attempted, but there was no response. The patient died 2 months after the onset of neurologic symptoms. We detected three distinct, rearranged regions of jc virus in the cerebellum, occipital lobe, and brainstem. These findings suggest that the brain lesions had three independent origins.
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keywords = bone
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6/23. Coats' plus: a progressive familial syndrome of bilateral Coats' disease, characteristic cerebral calcification, leukoencephalopathy, slow pre- and post-natal linear growth and defects of bone marrow and integument.

    In 1988 we reported two sisters with bilateral Coats' disease, sparse hair, dystrophic nails, and primeval splashes of intracranial calcification. We now provide an update on this family documenting the occurrence of skeletal defects comprising abnormal bone marrow, osteopenia, and sclerosis with a tendency to fractures, a mixed cerebellar and extrapyramidal movement disorder, infrequent epileptic seizures, leukodystrophic changes, and postnatal growth failure. Additionally, we present two previously unreported individuals from ireland and switzerland with the identical disorder which we designate Coats' plus. Since our original publication a number of other authors have described, frequently as a "new" syndrome, cases with a variable combination of the same features observed in our patients. We review this literature and suggest that the phenotypic overlap with dyskeratosis congenita may provide a clue to the molecular aetiology of this multisystem disorder.
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keywords = bone
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7/23. Fulminant inflammatory leukoencephalopathy associated with HAART-induced immune restoration in AIDS-related progressive multifocal leukoencephalopathy.

    HAART-induced immune restoration is beneficial for patients with AIDS-related progressive multifocal leukoencephalopathy (PML). However, in rare instances, an immune-reconstitution inflammatory syndrome (iris) may cause paradoxical clinical deterioration. We report the neuropathological study of an AIDS patient who presented with progressive cognitive deterioration; CD4( ) count was 117 and the HIV viral load >10(4); imaging showed non-enhancing lesions consistent with PML. Following initiation of HAART, CD4( ) was 300 and HIV viral load <10(3), but his neurological symptoms continued to deteriorate. Imaging revealed an increase in the size and number of lesions and enhancement of all the lesions. A stereotactic biopsy showed severe inflammatory and demyelinating lesions with marked infiltration by macrophages and T lymphocytes in the absence of a detectable infectious agent. Despite high doses of steroids, the patient died 3 months after admission. autopsy showed two types of lesions: (1) active inflammatory PML changes with abundant jc virus, and intraparenchymal and perivascular infiltration by T lymphocytes, and (2) acute perivenous leukoencephalitis devoid of jc virus. Most lymphocytes were CD8( ) lymphocytes; CD4( ) lymphocytes were virtually absent. Two pathological reactions were associated with the paradoxical clinical deterioration related to dysregulation of the immune response characteristic of iris in PML: (1) an accentuation of JCV infection, and (2) a nonspecific acute perivenous leukoencephalitis. We suggest that both these types of lesions are due to an imbalance of CD8( )/CD4( ) T cells, with massive infiltration of the cerebral parenchyma by CD8( ) cytotoxic T lymphocytes in the absence of sufficient CD4( ) response. Better understanding of the mechanisms of the iris may enable prevention or cure of this severe, sometimes fatal complication of HAART.
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8/23. Severe encephalitis resulting from coinfections with HIV and jc virus.

    We observed 3 cases of progressive multifocal leukoencephalopathy (PML) among frozen CNS samples obtained at autopsy from 102 adult AIDS patients. In 2 patients, PML was associated with severe HIV encephalitis. In those 2 cases, the areas of extensive JC-induced demyelination were massively infiltrated by HIV infected macrophages/microglial cells with evidence for localized increase of HIV encephalitis in PML lesions. Using immunohistochemistry and in situ hybridization, we demonstrated that each virus infects, in a latent or productive fashion, different CNS cell populations. Therefore, the extension of HIV encephalitis could not be related to an intracellular transactivation of 1 virus by the other. However, the results are consistent with dissemination of viral infection by the recruitment of HIV-infected macrophages to damaged areas of the brain. This phenomenon might be generalized to other pathogens that are frequently associated with HIV CNS infection. Early detection and treatment of opportunistic CNS lesions could be important to prevent extension of HIV encephalitis.
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9/23. Multifocal vacuolar leucoencephalopathy: a distinct HIV-associated lesion of the brain.

    A 20-year-old male AIDS patient developed rapidly progressive dementia for more than 3 months prior to death. autopsy showed, in addition to adrenal cytomegalovirus (CMV) infection and focal cerebral necrosis due to toxoplasmosis, multifocal subcortical white matter lesions of the brain which were strikingly similar to the histopathology of vacuolar myelopathy in AIDS. These distinct lesions contained macrophages which were rarely multinucleated and expressed HIV antigens by immunocytochemistry. The distribution of lesions mimics extrapontine myelinolysis and progressive multifocal leucoencephalopathy (PML); PML was excluded by the absence of papovaviruses by immunocytochemistry and by in situ dna hybridization. Tissue damage in multifocal vacuolar leucoencephalopathy is different from hitherto characterized HIV-specific neuropathology such as HIV encephalitis and HIV leucoencephalopathy, and should be included in the list of conditions with damage of the brain white matter in AIDS.
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10/23. Human immunodeficiency virus (HIV) and jc virus in acquired immune deficiency syndrome (AIDS) patients with progressive multifocal leukoencephalopathy.

    Of the 93 acquired immune deficiency syndrome (AIDS) patients autopsied between 1983 and 1986, 27 had evidence of viral encephalitis of which 3 had progressive multifocal leukoencephalopathy (PML), confirmed by electron microscopy. Using in situ hybridization with biotinylated jc virus probes, paraffin sections from the brains of these 27 patients were examined. jc virus was found only in those patients with histologically proven PML, while no evidence of jc virus was detected in the brains of the other 24 AIDS patients despite the presence of white matter pathology. brain biopsies of the PML patients demonstrated human immunodeficiency virus (HIV)-infected macrophages infiltrating regions of demyelination. When the patients died (2 to 6 months after diagnosis of PML), many more macrophages contained hiv antigens and some had fused to form multinucleated giant cells. These findings suggest that in AIDS patients, papovaviruses not only cause damage by directly infecting oligodendroglia but causes additional damage by eliciting the ingress of macrophages latently infected with HIV. As was seen with other infections (e.g., cytomegalovirus) of the CNS this might be a general mechanism of HIV entry into the brain.
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ranking = 1.5
keywords = macrophage
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