title: Role of cellular iron and oxygen in the regulation of HIV-1 infection.
abstract: Despite efficient antiretroviral therapy, eradication of HIV-1 infection is challenging and requires novel biological insights and therapeutic strategies. Among other physiological and environmental factors, intracellular iron greatly affects HIV-1 replication. Higher iron stores were shown to be associated with faster progression of HIV-1 infection and to inversely correlate with the survival of HIV-1 infected patients. Iron is required for several steps in the HIV-1 life cycle, including reverse transcription, HIV-1 gene expression and capsid assembly. Here, the authors present a comprehensive review of the molecular mechanisms involved in iron- and oxygen-mediated regulation of HIV-1 replication. We also propose key intracellular pathways that may be involved in regulating HIV-1 replication, via protein kinase complexes, CDK9/cyclin T1 and CDK 2/cyclin E, protein phosphatase-1 and other host factors.
authors.affiliation: Center for Sickle Cell Disease, Department of Medicine, Howard University, 520 W Street, NW, Washington DC 20059, USA.
authors.forename: Sergei
authors.initials: S
authors.lastname: Nekhai
authors.forename: Namita
authors.initials: N
authors.lastname: Kumari
authors.forename: Subhash
authors.initials: S
authors.lastname: Dhawan
keywords: CDK2; CDK9; HIV-1; Tat; hypoxia; iron chelators; protein phosphatase-1