Overexpression of Ki-67 and cyclins A and B1 in JC virus-infected cells of progressive multifocal leukoencephalopathy

Aurelio Ariza, José L. Mate, Marc Isamat, Ana Calatrava, Angela Fernández-Vasalo, José J. Navas-Palacios

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21 Citations (Scopus)


Both SV40 and JC virus (JCV) appropriate the host cell replicative machinery to attend to their own reproductive needs. SV40 large T antigert is able to induce the expression of cyclins A, B1, and E (but not of cylin D1) in transfected diploid cells. Whether JCV infection influences cyclin expression in a similar fashion in the setting of progressive multifocal leukoencephalopathy (PML) remains unknown. Brain lesions from 7 PML cases (4 autopsies and 3 biopsies) were immunohistochemically investigated for the expression of Ki-67 and cyclins A, B1, and D1. All 7 cases showed strong positivity for Ki-67 and cyclins A and B1 in JCV-infected oligodendrocytes and astrocytes, the nuclear immunolocalization of cyclin A being in strong contrast to the cytoplasmic distribution of cyclin B1. No immunostaining for cyclin D1 was obtained in any of the 7 cases. These findings suggest that JCV infection is associated with overexpression of Ki-67 and cyclins A and B1 in PML host glial cells. Since cyclin changes in JCV-infected cells recapitulate SV40 T antigen-associated cyclin fluctuations, it appears reasonable to think that JCV T antigert shares some of the previously described capabilities of SV40 T antigen to alter cyclin expression for the sake of viral replication.
Original languageEnglish
Pages (from-to)226-230
JournalJournal of Neuropathology and Experimental Neurology
Publication statusPublished - 1 Jan 1998


  • Cell cycle
  • Cyclins
  • Glial cells
  • JC virus
  • Ki-67
  • Progressive multifocal leukoencephalopathy.


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