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Semin Neurol. 2014 Feb;34(1):7-13. doi: 10.1055/s-0034-1372337. Epub 2014 Apr 8.

Evolving character of chronic central nervous system HIV infection.

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Department of Neurology, University of California, San Francisco, California.
Department of Neurology, Yale University, New Haven, Connecticut.
UNC Center for AIDS Research and the Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Division of Biological Chemistry, Biocenter, Innsbruck Medical University, Innsbruck, Austria.
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden and Institute of Neurology, Queen Square, London, United Kingdom.
Department of Infectious Diseases, University of Gothenburg, Gothenburg, Sweden.


Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system (CNS) begins early in systemic infection and continues throughout its untreated course. Despite a common cerebrospinal fluid inflammatory response, it is usually neurologically asymptomatic for much of this course, but can evolve in some individuals to HIV-associated dementia (HAD), a severe encephalopathy with characteristic cognitive and motor dysfunction. While widespread use of combination antiretroviral therapy (ART) has led to a marked decline in both the CNS infection and its neurologic severe consequence, HAD continues to afflict individuals presenting with advanced systemic infection in the developed world and a larger number in resource-poor settings where ART is more restricted. Additionally, milder CNS injury and dysfunction have broader prevalence, including in those treated with ART. Here we review the history and evolving nomenclature of HAD, its viral pathogenesis, clinical presentation and diagnosis, and treatment.

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