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PubMed1994

Brain and kidney of progressive multifocal leukoencephalopathy patients contain identical rearrangements of the JC virus promoter/enhancer.

The kidneys of six progressive multifocal leukoencephalopathy (PML) patients were examined by PCR amplification for the presence of JC virus. Amplification of three different areas of the viral genome from multiple samples of each kidney revealed three that were positive for the virus. The use of a PCR-based typing assay on all tissue samples, and cloned sequences from the viral coding region from each positive kidney showed that the same viral genome was present in the kidney as in the brain of the patient. Regulatory region clones all had the archetypal promoter/enhancer structure. However, when PCR fragments from the regulatory region were digested with a restriction enzyme which cuts in region D, the region most often deleted in PML-type promoters, a low level of undigested DNA remained. This DNA refractory to digestion had a rearranged sequence identical to that of the unique rearranged promoter in the brain of each patient.

Base Sequence↗
PubMed2000

The effect of potent antiretroviral therapy and JC virus load in cerebrospinal fluid on clinical outcome of patients with AIDS-associated progressive multifocal leukoencephalopathy.

A multicenter analysis of 57 consecutive human immunodeficiency virus-positive patients with progressive multifocal leukoencephalopathy (PML) was performed, to identify correlates of longer survival. JC virus (JCV) DNA was quantified in the cerebrospinal fluid (CSF) by polymerase chain reaction. Two months after therapy, 4% of the patients without highly active antiretroviral therapy (HAART) and 26% with HAART showed neurologic improvement or stability (P=.03), and 8% and 57%, respectively, reached undetectable JCV DNA levels in the CSF (P=.04). One-year probability of survival was.04 without HAART and.46 with HAART. HAART and lack of neurologic progression 2 months after diagnosis were independently associated with longer survival. Among HAART-treated patients, a baseline JCV DNA <4.7 log, and reaching undetectable levels after therapy predicted longer survival. Survival of AIDS-related PML is improved by HAART when JCV replication is controlled.

AIDS Dementia Complex↗
PubMed1984

Progressive multifocal leukoencephalopathy occurring with the acquired immune deficiency syndrome.

A 33-year-old homosexual man with symptoms and signs of a focal brain process was subsequently found to have an acquired immune deficiency syndrome (AIDS) with biopsy-proven progressive multifocal leukoencephalopathy. This report reemphasizes the association of progressive multifocal leukoencephalopathy with AIDS and probably is best viewed as another example of an opportunistic CNS infection complicating deficient cell-mediated immunity.

Acquired Immunodeficiency Syndrome↗
PubMed2004

[Progressive multifocal leukoencephalopathy confirmed by PCR for JC virus in cerebrospinal fluid: case report].

A case of progressive multifocal leukoencephalopathy (PML) is presented, with literature review. PML diagnosis and its differential diagnosis are presented, with emphasis on neuroradiology, cerebrospinal fluid analysis and polymerase chain reaction studies. The prognosis of PML is usually poor, with a median survival of 1-6 months. There is yet no proven effective treatment for this condition; HAART has become the standard of care for these patients.

AIDS-Related Opportunistic Infections↗
PubMed2001

Designs for clinical trials to test the efficacy of therapeutics in progressive multifocal leukoencephalopathy.

The design of a comparative treatment trial to evaluate the efficacy of therapeutics for progressive multifocal leukoencephalopathy (PML) is outlined. We propose a large simple randomized trial with patient survival as its primary endpoint, completed in a short period of time and involving a cohort with as few enrollment restrictions as possible. We use stratification as the counterweight to the lack of exclusion criteria and suggest that proper stratification will attenuate differences inherent in a heterogeneous subject cohort. Estimation of power, sample size, and study duration, implementation of interim analyses, toxicity management, and validation of secondary clinical measures are also addressed.

Antiviral Agents↗
PubMed1981

Isolation of a SV40-like virus from a patient with progressive multifocal leukoencephalopathy.

A SV40-like virus was isolated from the brain of a patient with progressive multifocal leukoencephalopathy. The virus was antigenically and serologically indistinguishable from SV40 wild type. A unique difference from SV40 was its ability to grow on human glial and CV-I monkey cells. The molecular weight of the viral DNA was very similar to that of SV40 DNA and the DNA cleavage patterns obtained after digestion with Hind II and Hind III restriction endonucleases were indistinguishable from those of SV40.

Adult↗
PubMed2003

Progressive multifocal leukoencephalopathy: diffusion-weighted imaging and pathological correlations.

We examined MRI of two patients with progressive multifocal leukoencephalopathy (PML), including diffusion-weighted imaging (DWI), with calculation of apparent diffusion coefficients (ADC). The pathology findings of one patient were compared with those of MRI. The lesions had different ADC and DWI appearances, depending on the stage of the disease. Newer lesions and the advancing edge of large lesions had normal-to-low ADC and gave high signal on DWI. Older lesions and the centre of large lesions had increased ADC and gave low signal. High signal on DWI and low ADC mark the regions of active infection and cell swelling, distinguishing them from areas of reparative gliosis.

Adult↗
PubMed1986

Progressive multifocal leukoencephalopathy: JC virus detection by in situ hybridization compared with immunohistochemistry.

In four cases of progressive multifocal leukoencephalopathy (PML), we compared biotin-labeled DNA:DNA in situ hybridization with peroxidase immunohistochemistry for the detection of JC virus (JCV). The localization of JCV DNA and JCV capsid protein was compared in formalin-fixed, paraffin-embedded brain tissues. Infected oligodendrocytes showed both JCV DNA and JCV protein. However, bizarre astrocytes demonstrated JCV capsid protein less often than JCV DNA. In situ hybridization with a biotinylated probe was as sensitive and specific as immunohistochemistry for diagnosis on formalin-fixed tissue. The presence of both JCV DNA and viral capsid protein in bizarre astrocytes suggests that these cells are neither truly transformed nor permissively infected, but are distinctively altered by JCV.

Adolescent↗
PubMed1997

JC virus regulatory region rearrangements and genotypes in progressive multifocal leukoencephalopathy: two independent aspects of virus variation.

JC virus (JCV) causes the central demyelinating disease progressive multifocal leukoencephalopathy (PML). JCV strains excreted in the urine are distinguishable from those in PML tissue by the configuration of their regulatory region to the right of ori: the archetypal regulatory region, 267 nucleotides long, is rearranged in PML tissue by deletion and duplication. Within the coding region JCV shows variations as a result of virus evolution. Four major genotypes are distinguishable of which Type 1 is based in Europe and Type 2 in Asia. Here, the regulatory region rearrangements and the viral genotypes of 29 JCV strains from PML brain were determined. Rearrangement patterns and genotypes were not associated. In general, deletions occurred before duplications, but exceptions to this rule exist. Each configuration of the 29 rearranged regulatory regions was unique and could be derived directly from the non-rearranged, archetypal form.

Gene Rearrangement↗
PubMed1993

Nonradioactive in situ hybridization in progressive multifocal leukoencephalopathy.

Biotinylated DNA:DNA in situ hybridization was used for determining the presence of JC virus in brain tissues of 67 patients thought to have progressive multifocal leukoencephalopathy. Sixty patients had acquired immunodeficiency syndrome (AIDS) or other illnesses that decreased the cell-mediated immunity. Two patients had no underlying disease, and five others had chronic illnesses not typically associated with reduced cell-mediated immunity. In situ hybridization with biotinylated probe provides specificity and ease of interpretation. The presence of virus can be correlated at the single-cell level with attendant pathologic changes in oligodendrocytes and astrocytes. Not only archival tissue but also tiny fragments of brain biopsy material can be evaluated successfully. Quantifying the technique suggests that the nucleus of a cell labeling for JC virus DNA averages 1,000 copies of replicating genome. Identification of an infected cell is pathologically significant even when only a few such cells are present in a biopsy specimen. Biotinylated DNA or RNA probes are equally effective in identifying infected cells. In situ hybridization will likely continue to be a useful adjunctive procedure for the evaluation of brain tissue from patients suspected of having progressive multifocal leukoencephalopathy.

Adult↗
PubMed2005

AIDS-related progressive multifocal leukoencephalopathy in the era of HAART: report of two cases and review of the literature.

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of the central nervous system. It is caused by the JC virus (JCV), a human polyomavirus replicating in human glial cells. PML is the result of the reactivation of latent JCV infection that usually occurs in the setting of cellular immunodeficiencies such as HIV-1 infection. Epidemiologic data suggest that the impact of highly active antiretroviral therapy (HAART) on the incidence of PML is less profound than seen with other opportunistic infections. Given the lack of an effective and specific therapy for PML, HAART remains the only therapeutic option in patients with PML. However, a significant number of cases appear unresponsive to antiretroviral therapy. Moreover, there is growing data on unexpected inflammatory cases of PML after initiation of HAART. Thus, PML will remain a relevant cause of morbidity and mortality in HIV- 1-infected patients. Here we report two cases of PML, along with a concise review of the literature on this important disease.

AIDS-Related Opportunistic Infections↗
PubMed1984

Emergence of papovavirus in long-term cultures of astrocytes from progressive multifocal leukoencephalopathy patients.

Primary and secondary cell cultures of brain tissue from two fatal cases of progressive multifocal leukoencephalopathy (PML) were closely monitored by light and electron microscopy and immunochemical labelling for glial fibrillary acidic protein. Although the cell cultures appeared heterogeneous and sometimes included fibroblasts, most of the cells were glial and many were identified as astrocytes by their morphology and immunochemical label. In long-term primary cultures four to four and a half months old and subcultures after many passages, focal cytopathic effect was noted in many cells. At the same time, papovavirions appeared in the nuclei of degenerating cells. However, the identity of these cells could not be established. Also, consistently present in the cultures were large atypical and pleomorphic cells that were likewise morphologically and immunochemically identified as astrocytes. Complete formed virions consistent with papovavirus appeared in the nuclei of some of these cells after several cell passages. The emergence of the virus in these cultured astrocytes supports the recently held notion that there may be in PML an abortive, or nonpermissive, papovavirus infection of this cell type which is believed to undergo cell transformation.

Aged↗
PubMed1986

Immunoenzymatic labelling of JC papovavirus T antigen in brains of patients with progressive multifocal leukoencephalopathy.

Formalin-fixed, paraffin-embedded autopsy sections of brains from two patients with progressive multifocal leukoencephalopathy (PML) were stained by peroxidase-antiperoxidase methods for human papovavirus T antigen, a nonstructural protein expressed in cells lytically infected or transformed by JC, BK, and SV40 viruses. Adjacent sections were stained for papovavirus common structural antigen, a component of JC, BK, and SV40 virions which is synthesized in productively infected but not transformed cells. Intense immunoperoxidase labelling specific for T antigen was detected in large numbers of oligodendrocytes at the edges of demyelinated areas and in occasional oligodendrocytes within otherwise normal brain. Occasional morphologically normal astrocytic cells exhibited similar specific staining, but only rate atypical astrocytic cells contained detectable amounts of T antigen. Examination of adjacent sections stained with antisera to common structural antigen revealed an identical pattern of immunoenzymatic labelling, indicating that most of the cells expressing T antigen were also expressing viral structural proteins. The present study demonstrates that T antigen can be identified by immunoperoxidase methods in routinely processed autopsy material from cases of PML, but that detectable amounts of antigen are found almost exclusively in cells undergoing lytic infection.

Adult↗