HIV TAT-mediated microglial senescence: Role of SIRT3-dependent mitochondrial oxidative stress.

ABSTRACT: The advent of combined antiretroviral treatment (cART) as a treatment for HIV-1 infection has not only resulted in a dramatic decrease in the peripheral viral load but has also led to increased life expectancy of the infected individuals. Paradoxically, increased lifespan is accompanied with higher prevalence of age-related comorbidities, including HIV-associated neurocognitive disorders (HAND). Present study was aimed at exploring the role of HIV TAT protein in mediating microglial mitochondrial oxidative stress, ultimately resulting in neuroinflammation and microglial senescence. Our findings demonstrated that exposure of mouse primary microglial cells (mPMs) to HIV TAT protein resulted in a senescence-like phenotype, that was characterized by elevated expression of both p16 and p21 prot

SUBMITTER: Thangaraj A 

PROVIDER: S-EPMC7779826 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature