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PubMed2007

Frequency and phenotype of JC virus-specific CD8+ T lymphocytes in the peripheral blood of patients with progressive multifocal leukoencephalopathy.

JC virus (JCV)-specific CD8+ cytotoxic T lymphocytes (CTL) are associated with a favorable outcome in patients with progressive multifocal leukoencephalopathy (PML) and cross-recognize the polyomavirus BK virus (BKV). We sought to determine the frequency and phenotype in fresh blood of CD8+ T cells specific for two A*0201-restricted JCV epitopes, VP1(p36) and VP1(p100), and assess their impact on JC and BK viremia and viruria in 15 healthy subjects, eight human immunodeficiency virus-positive (HIV+) individuals, and nine HIV+ patients with PML (HIV+ PML patients) classified as survivors. After magnetic pre-enrichment of CD8+ T cells, epitope-specific cells ranged from 0.001% to 0.022% [corrected] by tetramer staining, with no significant difference among the three study groups. By use of seven-color flow cytometry, there was no predominant differentiation phenotype subset among JCV-specific CD8+ T cells in healthy individuals, HIV+ subjects, or HIV+ PML patients. However, in one HIV+ PML patient studied in the acute phase, there was a majority of activated effector memory cells. BKV DNA was undetectable in all blood samples by quantitative PCR, while a low JC viral load was found in the blood of only one HIV+ and two HIV+ PML patients. JCV and BKV DNA were detected in 33.3% and 13.3% of all urine samples, respectively, independent of the presence of JCV-specific CTL. The detection of JCV DNA in the urine was associated with the presence of a JCV VP1(p100) CTL response. Immunotherapies aiming at increasing the cellular immune response against JCV may be valuable in the treatment of HIV+ individuals with PML.

Adult↗
PubMed2000

[Acquired immunodeficiency syndrome-associated progressive multifocal leukoencephalopathy treated with highly active anti-retroviral therapy].

We reported a patient with acquired immunodeficiency syndrome (AIDS)-associated progressive multifocal leukoencephalopathy (AIDS-PML), whose condition improved after highly active anti-retroviral therapy (HAART). A 70-year-old man was admitted to our hospital because of worsening left hemiplegia and disturbance of consciousness. During the past 30 years, he frequently traveled to the United States and southeast Asia. On neurological examination, he was somnolent and left hemiplegia with severe rigospasticity was present. The deep tendon reflexes showed hyper-reflexes with extensor plantar responses. Laboratory studies showed pancytopenia and positive HIV-1 antibodies. The CD4 cell count was 38/mm3 and his HIV viral RNA load in the blood was 9,500 copies/ml. T2-weighted magnetic resonance imaging (MRI) of the brain revealed asymmetrical high intensity white matter lesions in the right fronto-parietal, and left frontal regions and in the cerebellar hemisphere. The cerebrospinal fluid (CSF) protein elevated to 91 mg/dl with a normal cell count. The diagnosis of PML was confirmed by the detection of JC virus DNA in the CSF using a nested polymerase chain reaction assay. Three weeks after starting HAART with zidovudine, lamivudine, and indinavir, he was able to respond to simple commands. Two months later, the HIV viral RNA load decreased to less than 400 copies/mm3, and no JC virus DNA was detected in the CSF, with an increase of the CD4 cell count to 285/mm3 in the blood. A follow-up MRI of the brain showed a reduction in the cerebellar and cerebral white matter lesions. The recovering immune function by decreasing of the HIV load after HAART might suppress JC virus replication. It was suggested that HAART would become a beneficial treatment for patients with AIDS-PML.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Systemic infection by JC virus in non-HIV induced immunodeficiency without progressive multifocal leukoencephalopathy.

Reactivation of latent JC virus in immunodeficient subjects can lead to a demyelinating disease following lytic oligodendrocyte infection. It is known as idiopathic CD4+ lymphocytopenia and rarely occurs in immunosuppressed patients who are not infected by HIV. We describe a case of persistent idiopathic CD4+ lymphocytopenia in an HIV-negative 65-year-old woman. At autopsy, polymerase chain reaction analysis evidenced JC virus DNA in kidney, brain and liver although there were no signs of progressive multifocal leukoencephalopathy or evidence of oligodendrocyte infection. While her disease was not HIV-induced, it closely resembled AIDS in terms of the nature of the immune derangement and the clinical picture. The case also evidences the reactivation of JC virus infection in non-HIV-related immunosuppression in cerebral and/or extracerebral sites: liver infection seems to be particularly relevant since it has not yet been recognized as a common target of JC virus infection or a source of virus spreading. The absence of any sign of progressive multifocal leukoencephalopathy was remarkable: histological examination failed to disclose demyelination or other progressive multifocal leukoencephalopathy changes, and the search for JC virus DNA with in situ methods also gave negative results. The lack of lytic brain infection in this case would seem to support the hypothesis that the expression of progressive multifocal leukoencephalopathy is directly dependent on the presence of HIV infection.

Aged↗
PubMed1999

[Progressive multifocal leukoencephalopathy as a result of immunosuppressive therapy].

HISTORY AND ADMISSION FINDINGS: A 62-year-old woman developed paresis in her right arm within several weeks. She was being treated with methylprednisolone (4 mg daily) and chlorambucil (2 mg every other day) for systemic lupus erythematodes (SLE), which was now in remission. Neurological examination on admission revealed a right flaccid hemiparesis, predominantly of the right arm. The physical examination was otherwise unremarkable. INVESTIGATIONS: Magnetic resonance imaging (MRI) (T2 weighted) showed hyperintense changes in the subcortical medullary layer of the left precentral gyrus without perifocal oedema or abnormal contrast medium uptake, which argued against progressive cerebral ischaemia or tumour. Blood and cerebrospinal fluid (CSF) showed no abnormalities except leukopenia and a raised antinuclear antibody titre. Progressive paralysis of the right side of the body after 2 years of immunosuppressive treatment, the MRI findings and an essentially normal CSE suggested progressive multifocal leucoencephalopathy (PML), confirmed by polymerase chain reaction (PCR) demonstrating JC-virus DNA in serum and CSF. TREATMENT AND COURSE: As a result of the CNS infection with papovavirus JC, an opportunistic infection of the central nervous system, which is usually fatal, occurred. The cerebral changes spread within a few weeks, despite of the immunosuppressive drugs having been discontinued. The pareses progressed further and a marked personality disorder of organic origin ensued. CONCLUSION: While efficacious immunosuppressive drugs against autoimmune disease are available, their use risks the occurrence of life-threatening opportunistic infections.

Brain↗
PubMed2001

Reversal of CSF positivity for JC virus genome by cidofovir in a patient with systemic lupus erythematosus and progressive multifocal leukoencephalopathy.

We report the case of a 36-year-old woman affected by systemic lupus erythematosus who developed rapidly progressive multifocal leukoencephalopathy. Cidofovir therapy induced disappearance of JC virus genome from the cerebrospinal fluid and stabilization of the MRI picture. Despite the fatal outcome after a few months of disease, cidofovir treatment deserves further testing as single antiviral therapy in HIV-negative PML patients.

Adult↗
PubMed1985

Is progressive multifocal leukoencephalopathy associated with intrathecal IgG synthesis?

Examination of the cerebrospinal fluid by isoelectric focusing was done in 2 cases of progressive multifocal leukoencephalopathy (PML). The diagnosis was confirmed at autopsy in one case. IgG oligoclonal bands were found in both, suggesting that there was intrathecal immunoglobulin synthesis. Production may be due to a specific intrathecal response to papova virus or to IgG oligoclonal formation by lymphoma cells confined to the central nervous system or to a specific immune response to tumor cell antigens.

Aged↗
PubMed2006

A case report of progressive multifocal leukoencephalopathy in a human T-cell lymphotropic virus type 1-infected hemodialytic patient.

We experienced a case manifesting progressive multifocal leukoencephalopathy (PML) in a hemodialytic patient with hepatitis C virus-induced liver cirrhosis and human T-cell lymphotropic virus type-1 (HTLV-1)-associated uveitis. A 57-year-old male patient had received chronic hemodialysis therapy for 10 years, during which he received multiple blood transfusions and HTLV-1-associated uveitis developed. He complained of visual disturbance and disorientation. Brain CT scan showed diffuse and multifocal low density areas in occipital and temporal lobes, with gray matter relatively spared. MRI imaging showed high intensity lesions in the same areas. Cerebrospinal fluid culture was negative, but using nested PCR, rearranged regulatory region of JC virus DNA was detected. His consciousness level gradually deteriorated and complete paraplegia developed. Seven months after admission, he died of pneumonia. An autopsy confirmed the diagnosis of PML. Notably, mononuclear cell infiltration, gliosis and demyelinating lesions but no nuclear inclusion bodies were observed in the thoracic cord, which suggested HTLV-1-associated myelopathy. Because JC virus is activated under immunocompromised conditions, precipitating factors in this case appear multifactorial; depressed immune system induced by chronic hemodialysis as well as blood-borne hepatitis C virus/HTLV-1 infection might contribute to the activation of dormant JC virus and the development of florid clinical manifestation of PML.

Diffusion Magnetic Resonance Imaging↗
PubMed2006

Characteristics and antecedents of progressive multifocal leukoencephalopathy in an insured population.

Based on health insurance claims from a large U.S. health insurer, the authors identified 44 progressive multifocal leukoencephalopathy (PML) cases from 2002 through 2004 and described their characteristics, including antecedent diagnoses and treatments as well as survival. Immunosuppressive conditions such as HIV/AIDS, rather than potentially immunosuppressive treatments, were the main antecedents of PML. A lower mortality was observed among PML patients whose antecedent diagnosis was HIV/AIDS, the majority of whom received highly active antiretroviral therapy.

Adolescent↗