CCR5 antagonist reduces HIV-induced amyloidogenesis, tau pathology, neurodegeneration, and blood-brain barrier alterations in HIV-infected hu-PBL-NSG mice.

ABSTRACT:

Background

Neurocognitive impairment is present in 50% of HIV-infected individuals and is often associated with Alzheimer's Disease (AD)-like brain pathologies, including increased amyloid-beta (Aβ) and Tau hyperphosphorylation. Here, we aimed to determine whether HIV-1 infection causes AD-like pathologies in an HIV/AIDS humanized mouse model, and whether the CCR5 antagonist maraviroc alters HIV-induced pathologies.

Methods

NOD/scid-IL-2Rγ_c^null mice engrafted with human blood leukocytes were infected with HIV-1, left untreated or treated with maraviroc (120 mg/kg twice/day). Human cells in animal's blood were quantified weekly by flow cytometry. Animals were sacrificed at week-3 post-infection; blood and tissues viral loads were quantified using p24 ant

SUBMITTER: Bhargavan B 

PROVIDER: S-EPMC8607567 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature