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At least 235 records · Page 13Linked to original sources
PubMed1993

Re-evaluation of a case of progressive multifocal leukoencephalopathy previously diagnosed as simian virus 40 (SV40) etiology.

A case of progressive multifocal leukoencephalopathy (PML) reported previously to be of simian virus (SV40) etiology was re-evaluated. The supernatant from a 10% homogenate of brain material was inoculated into African green monkey kidney cells and BSC-1 cells which are permissive for SV40. However no cytopathic effect (CPE) developed and no virus was isolated. The brain supernatant agglutinated human group O erythrocytes and contained 5120 units/mL. The Hirt supernatant from the brain contained three DNA bands corresponding to forms I, II and III of circular double-stranded viral DNA. Restriction endonuclease cleavage analysis revealed that this viral DNA was different from SV40 DNA, but similar to JC virus DNA. After cloning of this viral DNA into pBR322 at the BamHI site, DNA homology of this virus and of SV40 was investigated. Cloned DNA from the brain hybridized with all the HpaI/EcoRI fragments of the SV40 genome at the effective temperature of Tm -50 degrees C [corrected]. At Tm -28 degrees C, however, the cloned DNA hybridized with only HpaI/EcoRI fragment B of the SV40 genome. In contrast to this, JC virus DNA hybridized with all five EcoRI/BamHI/HindIII fragments of cloned DNA even at Tm -28 degrees C. Therefore, the causative agent of this PML case was not SV40 but JC virus.

Cell Line↗
PubMed1998

Detection of JC virus in two African cases of progressive multifocal leukoencephalopathy including identification of JCV type 3 in a Gambian AIDS patient.

Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating central nervous system (CNS) infection, affecting mainly oligodendrocytes, but also occasional astrocytes. In the USA, Europe and Asia, PML is caused by the human polyomavirus JC virus (JCV) and in autopsy series occurs in about 4-7% of AIDS patients. In Africa, the prevalence of PML in AIDS patients is uncertain and the causative agent is unknown. This study reports immunocytochemical and PCR confirmation of PML in the CNS of an AIDS patient dying in Uganda, East Africa (case 1). In a Gambian patient infected with HIV-2 who died 3 months after onset of AIDS/PML in Germany (case 2), it was possible to confirm the identity of the virus by DNA sequencing of the PCR amplified JCV product. This African genotype of the virus (type 3) showed an unusual re-arrangement of the regulatory region, and could be distinguished at several sites from East African and African-American JCV strains described previously. This study has confirmed that PML is a complication of African AIDS as it is in Europe and the USA, and that JCV type 3 is pathogenic in African AIDS patients. Furthermore, the finding of an African genotype of JCV in a patient dying in Germany suggests that in this individual JCV represented a latent infection acquired in Africa.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Alpha Interferon in AIDS-Related Progressive Multifocal Leukoencephalopathy.

OBJECTIVE: To determine the efficacy of recombinant interferon alpha in the treatment of progressive multifocal leukoencephalopathy associated with the acquired immunodeficiency syndrome (AIDS). DESIGN: Open label, uncontrolled study. SETTING: Neurological unit and clinical AIDS program, Boston City Hospital, Boston, MA. PATIENTS: Four consecutive AIDS patients with pathologically confirmed progressive multifocal leukoencephalopathy. INTERVENTION: Each patient received alpha interferon for 4-12 weeks in a dose of 5-10 million units daily, administered subcutaneously. In addition, two of the four were taking acyclovir 2400 mg/day orally over the same period. RESULTS: None of the patients showed any clinical response to the therapy; the mean survival was 14 weeks. No adverse effects of the treatment were encountered. CONCLUSIONS: Despite anecdotal evidence that alpha interferon is effective in the treatment of progressive multifocal leukoencephalo pathy in non-AIDS patients, the experience of these patients suggests that the drug is of no benefit in AIDS-related PML.

AIDS-Related Opportunistic Infections↗
PubMed1983

Progressive multifocal leukoencephalopathy: a burnt-out case.

A patient with Hodgkin's disease developed progressive multifocal leukoencephalopathy (PML), documented by brain biopsy to be associated with JC virus infection. His disease progressed over several months, resulting in severe neurological deficit, but then stabilized with little or no further clinical progression during the remaining year of his life. Histopathological evaluation of the brain at autopsy supported the clinical impression that brain infection was arrested. Whereas the brain biopsy exhibited the histological features of active PML including giant bizarre astrocytes, at postmortem examination brain lesions appeared inactive, with regression of astrocytic changes and elimination of oligodendroglial inclusions. Similarly, JC virus antigen, present in the brain biopsy, was not detected in the autopsied brain. This case provides further evidence that PML is not invariably fatal and that clinical and cytological remission can occur.

Adult↗
PubMed1978

[Impaired visual perception in progressive multifocal leukoencephalopathy; a clinical diagnosis based on sequential computerized axial tomography (author's transl)].

Progressive multifocal leukoencephalopathy (PML) is a viral illness affecting principally cerebral white matter of patients, who have diminished immunologic resistance. A patient is presented, whose initial complaint was blurred vision. Relentless progression over a period of seven months to left hemianopsia, prosopagnosia, alexia with agraphia and eventually cortical blindness was observed. Accompanying the visual impairment was a steady deterioration of mental function. Sequential computerized axial tomography defined low density lesions in the occipital white matter with sparing of the cortical ribbon. As hemianopsia progressed to cortical blindness, the scans confirmed the evolution of bilaterial occipital lesions. The diagnosis was made clinically and established on histological and cultural grounds. Computerized tomography seems to be valuable in diagnosis and monitoring progress of PML.

Aged↗
PubMed1986

Progressive multifocal leukoencephalopathy complicating systemic lupus erythematosus.

Two patients with systemic lupus erythematosus who developed progressive multifocal leukoencephalopathy (PML) are described. Although the time of PML onset could not be determined with certainty, it probably developed after steroid-induced immunosuppression. However, high-dose corticosteroids appeared to produce transient amelioration in the neurologic disorder. We suggest that PML is an important addition to the list of conditions to be considered in the differential diagnosis when a patient with systemic lupus erythematosus develops neurologic abnormalities.

Adult↗
PubMedDate not supplied

[Progressive multifocal leukoencephalopathy. Role of imaging in its diagnosis. Perspectives].

We review five cases of Progressive Multifocal Leukoencephalopathy (PML), confirmed by biopsy in three cases and by LCR JC virus research by PCR (polymerase chain reaction) in two cases. We analysed the lesions and different forms of imagiological presentation, concerning location, mass effect, contrast enhancement and progress, and emphasize the importance of some atypical patterns. Reference is also made to the role of imaging in its diagnosis and new techniques, such as Spectroscopy and Transfer Magnetization, to avoid brain biopsy.

Adult↗
PubMed1999

Progressive multifocal leukoencephalopathy and JC virus genotypes in West African patients with acquired immunodeficiency syndrome: a pathologic and DNA sequence analysis of 4 cases.

OBJECTIVE: Progressive multifocal leukoencephalopathy is caused by polyomavirus JC in immunosuppressed patients. JC virus genotypes are identified by sequence analysis of the viral genome. Despite the prevalence of acquired immunodeficiency syndrome in sub-Saharan Africa, few cases of progressive multifocal leukoencephalopathy have been reported from this region. Here we describe 4 African cases and provide an analysis of viral genotypes. METHODS: Immunohistochemical staining by labeled streptavidin-biotin for capsid protein antigen was performed on all cases. Polymerase chain reaction amplification of viral genomic DNA was followed by direct cycle sequencing. RESULTS: JC virus type 3 was identified in 2 cases, and type 6 was isolated in 1 case. The viral regulatory region from 1 case showed an uncommon rearrangement pattern. CONCLUSIONS: Progressive multifocal leukoencephalopathy in West African patients with acquired immunodeficiency syndrome is caused by African genotypes of JC virus (types 3 and 6). The prevalence of disease in this autopsy series from sub-Saharan Africa (1.5%) was less than has been reported from Europe and the United States (4% to 10%) and may be partly due to biological differences in JC virus genotypes. Further studies will be needed to confirm this observation.

Acquired Immunodeficiency Syndrome↗