Journal
CURRENT HIV RESEARCH
Volume 4, Issue 3, Pages 307-318Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/157016206777709384
Keywords
HIV-1; neurotoxicity; apoptosis; neurodegeneration; demential
Categories
Funding
- NEI NIH HHS [R01 EY09024, R01 EY05477] Funding Source: Medline
- NICHD NIH HHS [P01 HD029587] Funding Source: Medline
- NINDS NIH HHS [R01 NS41207, R01 NS046994, R01 NS050621] Funding Source: Medline
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Infection with the human immunodeficiency virus-1 (HIV-1) and acquired immunodeficiency syndrome (AIDS) remain a persistent and even growing health problem worldwide. Besides its detrimental systemic effects on the immune system, HIV-1 seems to enter the brain very soon after peripheral infection and can induce severe and debilitating neurological problems that include behavioral abnormalities, motor dysfunction and frank dementia. Infected peripheral immune cells, in particular macrophages, appear to infiltrate the CNS and provoke a neuropathological response involving all cell types in the brain. Both viral and host factors, such as the viral strain and the response of the host's immune system, strongly influence the course of HIV-1 disease. Moreover, HIV-1-dependent disease processes in the periphery have a substantial effect on the pathology developing in the central nervous system (CNS), although the brain eventually harbors a distinctive viral population of its own. In the CNS, HIV-1 also initiates activation of chemokine receptors, inflammatory mediators, extracellular matrix-degrading enzymes and glutamate receptor-mediated excitotoxicity, all of which can activate numerous downstream signaling pathways and disturb neuronal and glial function. Although there have been substantial improvements in the control of viral infection in the periphery, an effective therapy for HIV-1 associated dementia (HAD) is,still not in sight. This article will review recently identified injurious mechanisms potentially contributing to neuronal death in association with HIV-1 disease and discuss recent and prospective approaches for therapy and prevention of HAD.
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