Repression of Nrf2/ARE regulated antioxidant genes and dysregulation of the cellular redox environment by the HIV Transactivator of Transcription.

ABSTRACT: Chronic HIV infection in the era of anti-retroviral therapy is associated with dramatically increased risk of developing severe cardio pulmonary disease. Common to these diseases is increased oxidative burden and chronic inflammation despite low viremia and restoration of CD4⁺ T-cell levels. Soluble viral factors are heavily implicated in these disease processes, including the HIV Transactivator of Transcription (Tat). Tat is produced in high levels during infection and secreted from infected cells into circulation where it is internalized by bystander cells and is known to regulate inflammatory pathways and elicit a pro-oxidant environment. We have examined the effects of Tat on the anti-oxidant regulatory network driven by the transcription factor Nuclear factor (erythroid-der

SUBMITTER: Simenauer A 

PROVIDER: S-EPMC7096131 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature