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Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of the human CNS caused by polyomavirus JC.1 Its characteristic pathologic features include lytic infection of oligodendrocytes, with typical nuclear inclusions, formation of large bizarre astrocytes, and demyelination. PML is common in immunosuppressed individuals and is the third most frequent neurologic complication in HIV-infected patients in the era of highly active antiretroviral therapy (HAART).2 Except for HAART, no therapy has been demonstrated to be effective against PML; the efficacy of cidofovir, a nucleotide analogue that inhibits the replication of simian polyomavirus in vitro, is controversial.
Selected reports demonstrate that in patients with AIDS, PML can occur early after the introduction of HAART during the phase of recovery of the immune system. These cases are sometimes associated with inflammatory reaction as shown by the presence of perivascular lymphomonocytic infiltrates or contrast enhancement on neuroimaging studies and show variable clinical outcomes.3–6⇓⇓⇓ In this …
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