Abstract
Human immunodeficiency virus type 1 (HIV-1) over the past 25 years has become a chronic disease in the developed world that is treatable by antiretroviral therapy but is incapable of being eradicated due to a subpopulation of cells that escape the immune system and therapies and become latently infected. This chapter discusses molecular mechanisms surrounding the development of latency, both pre- and post-integration of the proviral genome and the maintenance of latency, including the role of nucleotide levels, adenosine triphosphate (ATP), levels of certain host transcription factors (NF-κB and NFAT) as well as viral proteins (Vif and Tat), and the chromatin architecture. Also discussed are the cellular reservoirs involved in latency, including the memory CD4+ T cells, which have been proposed as one of the main latent cellular reservoirs, the monocyte–macrophage cell lineage and its role in both HIV-1 latency in the bone marrow, peripheral blood, and CNS, and other cells of the CNS such as the microglial cells and the astrocytes. Finally, the role of latency in neuropathogenesis and reseeding of the peripheral blood from these viral reservoirs are discussed.
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References
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These studies were funded in part by the Public Health Service, National Institutes of Health through grants (B. Wigdahl, Principal Investigator) from the National Institute of Neurological Disorders and Stroke, NS32092 and NS46263, and the National Institute of Drug Abuse, DA19807
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Banerjee, A., Nonnemacher, M.R., Wigdahl, B. (2010). HIV Latency and Reactivation: Role in Neuropathogenesis. In: Meucci, O. (eds) Chemokine Receptors and NeuroAIDS. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-0793-6_5
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