The primary cause of HIV encephalopathy (HIVE) is the infection of the CNS caused by HIV. If untreated, 15-20 % of patients will eventually develop HIVE. Since the introduction of highly active antiretroviral therapy (HAART) the incidence of the disorder has decreased. Other terms used for this condition with largely the same significance are AIDS dementia complex, AIDS dementia, and HIV-associated cognitive motor complex. HIVE only occurs in the later stages of HIV infection when there is a profound immune suppression (CD4 count below 200/^l). The incidence of HIVE will likely increase in developed countries as a consequence of increasing life expectancy (Valcour 2004).
In HIVE, there is a high level of replication of HIV in macrophages and microglial cells of the brain. Neuronal cells have not been shown to be infected. However, different immunopathological mechanisms lead to functional and structural damage of these cells. With respect to viral replication and viral quasispecies, the CNS is partially independent from the hematolymphatic compartment (Eggers 2003). The viral load in the brain parenchyma and the cerebrospinal fluid has been shown to be high in HIVE, and loosely correlates with the extent of the disease.
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