Journal
CURRENT HIV RESEARCH
Volume 4, Issue 3, Pages 267-278Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/157016206777709500
Keywords
HIV; CCR5; macrophages; microglia; neurotropism
Categories
Funding
- NIAID NIH HHS [AI054207] Funding Source: Medline
- NIDA NIH HHS [DA16549] Funding Source: Medline
- NINDS NIH HHS [NS35734, NS37277] Funding Source: Medline
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Human immunodeficiency virus type 1 (HIV) infects macrophages and microglia in the CNS and frequently causes neurocognitive impairment. Although antiviral therapy generally reduces the viral load in the CNS and improves HIV-associated neurological dysfunction, most current antiviral drugs have poor CNS penetrance and cannot completely suppress viral replication. Furthermore, drug-resistance mutations can evolve independently in the CNS. Thus, a long-lived viral reservoir persists in macrophages and microglia in the brain despite antiviral therapy. This review discusses mechanisms underlying the neurotropism of HIV, focusing on the role of the HIV envelope glycoproteins and their interactions with CD4 and the chemokine receptors CCR5 and CXCR4. We review data from studies of neurotropic HIV derived from the brains of patients with HIV-associated neurocognitive impairment as well as studies of nonhuman primate models. Understanding mechanisms that underlie HIV neurotropism and neurovirulence is critical for development of therapeutics to inhibit CNS infection and preventing neurological injury in HIV-infected individuals.
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