Journal of Neuroimmune Pharmacology

, Volume 4, Issue 2, pp 175–189

Host and Viral Factors Influencing the Pathogenesis of HIV-Associated Neurocognitive Disorders

Authors

  • Suman Jayadev
    • Department of Neurology and Center for Neurogenetics and NeurotherapeuticsUniversity of Washington
    • Department of Neurology and Center for Neurogenetics and NeurotherapeuticsUniversity of Washington
Invited Review

DOI: 10.1007/s11481-009-9154-6

Cite this article as:
Jayadev, S. & Garden, G.A. J Neuroimmune Pharmacol (2009) 4: 175. doi:10.1007/s11481-009-9154-6

Abstract

The human immunodeficiency virus (HIV) invades the central nervous system early in the course of infection and establishes a protected viral reservoir. However, neurocognitive consequences of HIV infection, known collectively as HIV-associated neurocognitive disorders (HAND), develop in only a small portion of infected patients. The precise mechanisms of pathogenesis involved in HIV-induced central nervous system injury are still not completely understood. In particular, most theories of HAND pathogenesis cannot account for either the selective vulnerability of specific neuronal populations to HIV-induced neurodegeneration or why only a subset of patients develop clinically detectable nervous system disease. Epidemiological and virological studies have identified a variety of host and viral factors that are associated with increased risk of developing HAND. Some host factors that predispose HIV-infected patients to HAND overlap with those associated with Alzheimer’s disease (AD), suggesting the possibility that common pathogenic mechanisms may participate in both diseases. Here, we will review reports of host and viral factors associated with HAND and place these studies in the context of the data employed to support current theories regarding the molecular and cellular mechanisms that lead to HIV-induced neurodegeneration with additional focus on mechanisms common to AD pathogenesis.

Keywords

HIVHIV-associated neurocognitive disordersAlzheimer’s diseaseinflammationautophagysynapto-dendritic degeneration

Copyright information

© Springer Science+Business Media, LLC 2009