THE NEUROLOGICAL manifestations of human immunodeficiency virus (HIV) infection are a major source of morbidity and mortality despite advances in antiretroviral therapy. Viral invasion of the central nervous system (CNS) occurs as an extremely early event following HIV infection,1,2 yet, generally, productive infection is uncommon until later in HIV/acquired immunodeficiency syndrome (AIDS), after the development of immunosuppression.3 In approximately 10% of patients, initial (acute) HIV infection is associated with acute self-limited meningitis or encephalitis, although it more characteristically presents as a mild flu- or mononucleosis-like illness.4,5 Using highly sensitive polymerase chain reaction techniques to amplify viral RNA from cerebrospinal fluid (CSF), it is possible to detect evidence of HIV infection of the CNS in virtually all untreated, asymptomatic individuals.6-9 Once in the CNS,10 HIV establishes a chronic progressive infection that predominantly involves monocytes, perivascular macrophages, and microglial cells, and, to some extent, a restricted infection of astrocytes.11,12
Tyler KL, McArthur JC. Through a Glass, Darkly: Cerebrospinal Fluid Viral Load Measurements and the Pathogenesis of Human Immunodeficiency Virus Infection of the Central Nervous System. Arch Neurol. 2002;59(6):909–912. doi:10.1001/archneur.59.6.909
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