The pathogenesis of HIV-associated dementia is at present incompletely understood. In the brain, productive infection is almost exclusively restricted to macrophages and microglia. Neuronal injury (most probably apoptosis) is currently believed to be produced by toxic products released directly by HIV-infected macrophages and microglia or by activated astrocytes. Some of these factors have been identified: they include the platelet-activating factor, quinolinic acid, nitric oxide, and some metabolites of arachidonic acid, which are neurotoxic, and tumour necrosis factor-a, which is toxic for oligodendrocytes and can cause demyelination.

The strains of HIV which are isolated from the brain have in common the characteristic of infecting macrophages but not lymphocytes. This macrophage tropism corresponds to what was initially regarded as neurotropism. Macrophage tropism is related to a mutation in a specific region of gp120, the external glycoprotein of the virus. In the late stages of the infection, when active replication of the virus generates more mutants and the compromised immune system permits the escape of these mutants, the development of macrophage-trophic strains is more likely to occur, and this probably represents the limiting step for the occurrence of HIV encephalopathy and dementia/!1

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