Journal
INFECTION GENETICS AND EVOLUTION
Volume 11, Issue 1, Pages 31-37Publisher
ELSEVIER
DOI: 10.1016/j.meegid.2010.10.016
Keywords
HIV; Brain; Dementia; Meninges; Viral migration; Macrophages; HIV-associated disease pathologies
Categories
Funding
- NIH [U01 CA066529, U19 MH081835, R01 NS063897-01A2, CA-09126]
- NATIONAL CANCER INSTITUTE [T32CA009126, U01CA066529] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [U19MH081835] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS063897] Funding Source: NIH RePORTER
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Brain infection by the human immunodeficiency virus type 1 (HIV-1) has been investigated in many reports with a variety of conclusions concerning the time of entry and degree of viral compartmentalization. To address these diverse findings, we sequenced HIV-1 gp120 clones from a wide range of brain. peripheral and meningeal tissues from five patients who died from several HIV-1 associated disease pathologies. High-resolution phylogenetic analysis confirmed previous studies that showed a significant degree of compartmentalization in brain and peripheral tissue subpopulations. Some intermixing between the HIV-1 subpopulations was evident, especially in patients that died from pathologies other than HIV-associated dementia. Interestingly, the major tissue harboring virus from both the brain and peripheral tissues was the meninges. These results show that (1) HIV-1 is clearly capable of migrating out of the brain, (2) the meninges are the most likely primary transport tissues, and (3) infected brain macrophages comprise an important HIV reservoir during highly active antiretroviral therapy. (C) 2010 Elsevier B.V. All rights reserved.
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