Up-regulation of MAP2e-expressing oligodendrocytes in the white matter of patients with HIV-1 encephalitis.

HIV-1 encephalitis (HIVE) is characterized by infection of macrophages and microglial cells, diffuse gliosis, and damage to neuronal populations. The nature of the white matter damage in HIVE remains elusive, and little is known about the status of the oligodendrocyte in HIVE. We have recently described a novel isoform of microtubule-associated protein-2 (MAP2e), which is expressed transiently in developing oligodendrocytes during myelination, and in remyelinating oligodendrocytes in multiple sclerosis lesions. In this study, we tested the hypothesis that MAP2e expression would be increased in the white matter of HIVE. We analysed brain sections from patients with HIVE and controls (HIV+ and HIV-) by immunocytochemistry and found that MAP2e+ cells are significantly increased in HIVE (range, 5-167 cells per cm2) compared to controls (range, 1-25 cells per cm2). MAP2e+ cells were negative for GFAP, CD68, LN3, RCA-1, von Willebrand factor and HIV-1 p24, but positive for MBP or Luxol-Fast Blue, supporting their oligodendroglial lineage. A topographical association between MAP2e and HIV-1 p24 expression was noted, but not between MAP2e and beta-APP, a marker of damaged axons. Our results demonstrate that MAP2e can serve as a marker of white matter damage in HIVE and support the notion that oligodendrocyte damage/repair occurs during HIV-1 infection.