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JC virus persistence following progressive multifocal leukoencephalopathy in multiple sclerosis patients treated with

Caroline F Ryschkewitsch1, Peter N Jensen, Maria Chiara Monaco

  • 1Laboratory of Molecular Medicine and Neuroscience, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.

Annals of Neurology
|September 7, 2010
PubMed

Insights

JC virus (JCV) DNA detection in cerebrospinal fluid (CSF) confirms progressive multifocal leukoencephalopathy (PML). JCV DNA can persist in CSF even after treatment, indicating the virus may not be fully cleared.

Area of Science:

  • Neurovirology
  • Immunology
  • Clinical Neurology

Background:

  • JC virus (JCV) DNA in CSF is crucial for diagnosing progressive multifocal leukoencephalopathy (PML).
  • Natalizumab treatment for multiple sclerosis (MS) is associated with an increased risk of PML.
  • Understanding JCV persistence is vital for managing PML, especially in immunocompromised patients.

Purpose of the Study:

  • To investigate the persistence of JCV DNA in CSF of natalizumab-treated MS patients diagnosed with PML.
  • To analyze anti-JCV antibody levels in relation to JCV DNA persistence and disease course.
  • To evaluate the long-term viral shedding and neurological outcomes in PML patients.

Main Methods:

  • Confirmatory laboratory diagnosis of PML using JCV DNA detection in CSF samples.
  • Longitudinal analysis of multiple CSF samples from PML patients.
  • Measurement of specific anti-JCV antibodies in plasma/sera.
  • Monitoring of clinical status, including immune reconstitution inflammatory syndrome (IRIS) and neurological deficits.

Main Results:

  • JCV DNA was detected in the CSF of 35 natalizumab-treated MS patients diagnosed with PML.
  • Seven of 13 patients showed persistent JCV DNA in CSF despite treatments like IRIS, plasma exchange, and immunoabsorption.
  • Most patients exhibited moderate to high or rising anti-JCV antibody levels, though some had atypical serological profiles at diagnosis.
  • Viral persistence and neurological deficits continued for several years in some cases.

Conclusions:

  • JCV DNA can persist in the CSF of PML patients even after therapeutic interventions.
  • The findings suggest that JCV infection may not be completely cleared, even with immune reconstitution.
  • Long-term viral persistence highlights the challenges in managing PML and its associated neurological sequelae.

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