Association of simian virus 40 with a central nervous system lesion distinct from progressive multifocal leukoencephalopathy in macaques with AIDS.
(1/318)
The primate polyomavirus SV40 is known to cause interstitial nephritis in primary infections and progressive multifocal leukoencephalopathy (PML) upon reactivation of a latent infection in SIV-infected macaques. We now describe a second central nervous system manifestation of SV40: a meningoencephalitis affecting cerebral gray matter, without demyelination, distinct from PML. Meningoencephalitis appears also to be a primary manifestation of SV40 infection and can be seen in conjunction with SV40-induced interstitial nephritis and pneumonitis. The difference in the lesions of meningoencephalitis and PML does not appear to be due to cellular tropism, as both oligodendrocytes and astrocytes are infected in PML and meningoencephalitis, as determined by in situ hybridization or immunohistochemistry for SV40 coupled with immunohistochemistry for cellular determinants. This is further supported by examination of SV40 nucleic acid sequences from the ori-enhancer and large-T-antigen regions, which reveals no tissue-or lesion-specific variation in SV40 sequences. (+info)
Immunohistochemical detection of JC virus in nontumorous renal tissue of a patient with renal cancer but without progressive multifocal leukoencephalopathy.
(2/318)
We performed immunohistochemical staining on the nontumorous renal tissue of 45 patients with renal cancer but without progressive multifocal encephalopathy using JCV-specific antibody. For one patient we found positive staining of the nuclei of the renal collecting ducts. Immunoelectron microscopic examination of the positive cell nuclei revealed electron-dense polyomavirus-like particles. (+info)
Progressive multifocal leukoencephalopathy after autologous bone marrow transplantation and alpha-interferon immunotherapy.
(3/318)
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. (+info)
Progressive multifocal leucoencephalopathy with peripheral demyelinating neuropathy after autologous bone marrow transplantation for acute myeloblastic leukemia (FAB5).
(4/318)
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. (+info)
Clinical and virological monitoring during treatment with intrathecal cytarabine in patients with AIDS-associated progressive multifocal leukoencephalopathy.
(5/318)
We describe the clinical and virological outcome of human immunodeficiency virus-infected patients with progressive multifocal leukoencephalopathy (PML) treated with cytarabine. Twenty-seven patients received intrathecal cytarabine, 5 received concomitant intravenous cytarabine, and 20 received concomitant antiretroviral therapy. The median baseline CD4+ cell count was 28/mm3. After 4 weeks, 4 (19%) of 21 evaluable patients had stable disease, whereas the others progressed. The median survival from diagnosis and from onset was 66 and 128 days, respectively. Patients with Karnofsky scores of >50 and those previously taking antiretroviral medications had a higher probability of survival 3 months after diagnosis (P = .003 and P = .05, respectively). Overall, after 4 weeks, median JC virus load in CSF increased by 0.7 log10 copies/mL from baseline (P = NS). The mean JC virus load at 4 weeks was lower in patients with stable disease than in progressors (3.47 vs. 4.47 log10 copies/mL; P = .027). JC virus became undetectable in the only patient who had a long-term stable condition. The concentration of JC virus in CSF showed a correlation with clinical outcome. (+info)
Proton magnetic resonance spectroscopy pattern of progressive multifocal leukoencephalopathy in AIDS.
(6/318)
The objective was to determine whether the use of intermediate echo times (135 ms) in proton magnetic resonance spectroscopy (1H-MRS) detects a homogenous pattern in progressive multifocal leukoencephalopathy (PML) in HIV-1 infected people, and to confirm the results of previous studies. Six patients infected with HIV-1, with PML established by biopsy, and six healthy age and sex matched volunteers were evaluated to define their spectroscopic pattern. 1H-MRS spectra performed at 1.5 T were obtained with the STEAM sequence: TE/TM/TR, 20 ms/13.7 ms/2000 ms; 2500 Hz, size 2048 points, 256 acquisitions (STEAM-20) and with the PRESS sequence; TE/TR, 135 ms/2000 ms; 2500 Hz, size 2048 points, 256 acquisitions (PRESS-135). A single voxel was placed on the lesions and on the parieto-occipital white matter of controls. The peaks of N-acetylaspartate (NAA), choline (Cho), myoinositol (mI), lactate, and lipids were considered, and the results were expressed using creatine as reference. Spectra of PML lesions were characterised by significantly reduced NAA, lactate presence, and by significantly increased Cho and lipids compared with control group values. These results indicate that 1H-MRS detects a homogenous pattern in PML lesions. Recent studies, together with this, suggest that 1H-MRS may help in the diagnostic approach to patients with suspected PML lesions associated with AIDS. (+info)
Archetypal and rearranged sequences of human polyomavirus JC transcription control region in peripheral blood leukocytes and in cerebrospinal fluid.
(7/318)
Two forms of human polyomavirus JC (JCV) genome are known based upon the structure of the transcriptional control region (TCR) of the virus: the archetypal form, which is commonly detected in urine, and the rearranged form, which was first detected in brain tissue from progressive multifocal leukoencephalopathy (PML) patients. The latter actually includes a group of TCR variants that, relative to the former, are characterized by various deletions and/or duplications. The aim of this study was to establish whether or not a correlation exists among the TCR type, the spreading of the virus within the host and its ability to cause PML. JCV TCR sequences from peripheral blood leukocytes (PBL) and cerebrospinal fluid (CSF) obtained from various groups of patients were compared. JCV with archetypal TCR was detected in CSF and PBL specimens from patients without neurological disorders or who eventually received a diagnosis of a non-PML neurological disorder. Rearranged TCR sequences were detected in all the CSF and PBL specimens from PML patients. The high similarity observed between the TCR structure detected in PBL and CSF specimens from individual patients could strengthen the hypothesis that PBL has a role in spreading JCV to the brain. Moreover, heterogeneous TCR patterns have been shown in individual PBL specimens from PML patients. This supports the hypothesis that, in PBL, JCV may replicate and undergo rearrangements of the TCR. The detection of JCV DNA by PCR in CSF independently from PML, although rare, could suggest that this assay is not sufficient for a virological diagnosis of PML. Further studies are required to assess the usefulness of quantitative assays or TCR typing in combination with PCR for diagnostic purposes. (+info)
Progressive multifocal leukoencephalopathy in a patient with acquired immunodeficiency syndrome (AIDS) manifesting Gerstmann's syndrome.
(8/318)
We reported a case of acquired immunodeficiency syndrome (AIDS) via multiple blood transfusions, who manifested progressive multifocal leukoencephalopathy (PML) about 18 months after the development of AIDS. PML initiated with right hemiparesis, dysphasia, and Gerstmann's syndrome and resulted in death within 2 months after the onset. Neuroimaging examinations revealed white matter lesions mainly in the left posterior parietal lobe. The cortical gray matter also showed abnormal signal intensity. Peripheral CD4+ lymphocyte count was 81/microl. Routine cerebrospinal fluid (CSF) examinations were negative. CSF antibodies against herpes simplex virus, varicella-zoster virus, cytomegalovirus, Epstein-Barr virus as well as serum antibody against toxoplasma gondii were negative. Though autopsy or biopsy of the brain was not performed, JC virus genomes were detected in the CSF sample by a polymerase chain reaction, and their sequencing showed unique alterations of the regulatory regions, characteristic to PML-type JC virus. (+info)