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- W2744214718 abstract "The widespread use of combinational antiretroviral therapies (cART) in developed countries has changed the course of Human Immunodeficiency Virus (HIV) infection from an almost universally fatal disease to a chronic infection for the majority of individuals. Although cART has reduced the severity of neurological damage in HIV-infected individuals, the likelihood of cognitive impairment increases with age, and duration of infection. As cART does not suppress the expression of HIV non-structural proteins, it has been proposed that a constitutive production of HIV regulatory proteins in infected brain cells may contribute to neurological damage. However, this assumption has never been experimentally tested. Here we take advantage of the leaky tetracycline promoter system in the Tat-transgenic mouse to show that a chronic very low-level expression of Tat is associated with astrocyte activation, inflammatory cytokine expression, ceramide accumulation, reductions in brain volume, synaptic, and axonal damage that occurs over a time frame of 1 year. These data suggest that a chronic low-level production of Tat may contribute to progressive neurological damage in virally suppressed HIV-infected individuals." @default.
- W2744214718 created "2017-08-17" @default.
- W2744214718 creator A5002913273 @default.
- W2744214718 creator A5014301291 @default.
- W2744214718 creator A5019952857 @default.
- W2744214718 creator A5022491794 @default.
- W2744214718 creator A5040337172 @default.
- W2744214718 creator A5076458805 @default.
- W2744214718 creator A5084785068 @default.
- W2744214718 creator A5086584939 @default.
- W2744214718 date "2017-08-10" @default.
- W2744214718 modified "2023-10-18" @default.
- W2744214718 title "Chronic low-level expression of HIV-1 Tat promotes a neurodegenerative phenotype with aging" @default.
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