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Isolation of Brain-infiltrating Leukocytes
06:44

Isolation of Brain-infiltrating Leukocytes

Published on: June 13, 2011

Effects of JC virus infection on anti-apoptotic protein survivin in progressive multifocal leukoencephalopathy

Sergio Piña-Oviedo1, Katarzyna Urbanska, Sujatha Radhakrishnan

  • 1Department of Neuroscience, Neuropathology Core, Temple University School of Medicine, 1900 North 12th St., Suite 240, Philadelphia, PA 19122, USA.

The American Journal of Pathology
|March 30, 2007
PubMed

Insights

JC virus (JCV) infection in progressive multifocal leukoencephalopathy (PML) hijacks the anti-apoptotic protein survivin. Inhibiting survivin increased apoptosis in infected cells, suggesting new therapeutic strategies for PML.

Area of Science:

  • Neurovirology
  • Cellular Biology
  • Pathology

Background:

  • Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease caused by JC virus (JCV) infection of oligodendrocytes.
  • Viruses can manipulate host cell apoptosis pathways for replication; survivin, an inhibitor of apoptosis protein, is typically absent in differentiated cells.

Purpose of the Study:

  • To investigate the role of survivin in JCV infection and PML pathogenesis.
  • To determine if JCV up-regulates survivin and if this contributes to reduced apoptosis.

Main Methods:

  • Immunohistochemistry on 20 PML cases to detect survivin.
  • Infection of oligodendroglial and astrocytic cultures with JCV.
  • Cell cycle analysis and DNA laddering to assess apoptosis.
  • Small interfering RNA (siRNA) to inhibit survivin expression.

Main Results:

  • Survivin was detected in JCV-infected oligodendrocytes and astrocytes in PML lesions.
  • JCV infection of glial cultures led to increased survivin expression and reduced apoptosis.
  • siRNA-mediated inhibition of survivin significantly increased apoptosis in JCV-infected cells.

Conclusions:

  • JCV infection activates survivin in oligodendrocytes and astrocytes, contributing to its survival by inhibiting apoptosis.
  • Survivin up-regulation represents a novel anti-apoptotic mechanism employed by JCV.
  • Targeting survivin may offer a potential therapeutic strategy for PML.

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