Alterations of redox and iron metabolism accompany development of HIV latency

ABSTRACT: HIV-1 persists in a latent form during antiretroviral therapy, mainly in CD4+ T cells, thus hampering efforts for a cure. HIV-1 infection is accompanied by metabolic alterations, such as oxidative stress, but the effect of cellular antioxidant responses on viral replication and latency is unknown. Here, we show that cells survive retroviral replication, both in vitro and in vivo in SIVmac infected macaques, by upregulating antioxidant pathways and the intertwined iron import pathway. These changes are associated with remodeling of promyelocytic leukemia protein nuclear bodies (PML NBs), an important constituent of nuclear architecture and a marker of HIV-1 latency. We found that PML NBs are hyper SUMOylated and that PML protein is degraded via the ubiquitin-proteasome pathway in productive

SUBMITTER: Dr. Iart Luca Shytaj 

PROVIDER: S-SCDT-EMBOJ-2019-102209 | biostudies-other |

REPOSITORIES: biostudies-other