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.

Incidence of Human Immunodeficiency Virus in Sickle Cell Patients in the Cape Coast Metropolis, Ghana

“…This could support the studies of some researchers which suggested that HIV infection progresses slowly in patients with sickle cell disease (SCD) [6] [9]. SCD is associated with upregulated inflammatory and haemolytic pathways which lead to the suggestion that the disease may influence the course of HIV infection and progression [6] [8].…”

“…A few studies conducted suggested that HIV infection progresses slowly in patients with sickle cell disease (SCD) [6]- [8]. Further studies have also revealed that Sickle Cell trait patients are associated with low frequency of HIV diagnosis [9]. A study of HIV infection through blood transfusion in children with Sickle Cell Anaemia in Nigeria and Congo were 2.9% and 2.6% respectively [10] [11].…”

Short Communication: High Cellular Iron Levels Are Associated with Increased HIV Infection and Replication

“…[7][8][9] In vitro studies also provided conflicting evidence linking iron with HIV progression. Higher cellular iron levels in HIV-infected macrophages are associated with increasing HIV transcription, 10,11 and treatment of monocytes with the iron chelator deferoxamine (DFO) decreased NF-jB and HIV-1 reactivation by oxidative stress. 12 However, another study found no change in NF-jB with iron chelation.…”

“…12 However, another study found no change in NF-jB with iron chelation. 13 A reduction in cyclin-dependent kinase (CDK) 2/cyclin E complex activity has also been suggested as one of the mechanisms of how iron deficiency reduces HIV replication, 11,14 but changes in CDK2/cyclin E complex activity were not observed in another study using DFO to decrease cellular iron. 15 Therefore, the interaction between HIV infection and cellular and systemic iron status, particularly in the post-ART era, remains unclear.…”

Alteraciones del crecimiento y en el estado nutricional de pacientes pediátricos infectados con VIH

“…9 Sin embargo, tras aumentar la supervivencia de los pacientes y por el tiempo de administración de los medicamentos antirretrovirales, se han observado efectos adversos como las dislipidemias que pueden implicar factores de riesgo cardiovascular en pacientes con VIH. 25,26 Existen varios estudios que respaldan lo descrito previamente. Por ejemplo, en un estudio realizado en Uruguay por Gutiérrez y sus colegas, que evaluó la prevalencia de dislipidemias en niños VIH positivos con tratamiento antirretroviral, encontraron que 55% tuvo alguna alteración en las concentraciones totales de colesterol, triglicéridos, o ambos.…”