HIV-1 Tat-induced microgliosis and synaptic damage via interactions between peripheral and central myeloid cells.

ABSTRACT: Despite the ability of combination antiretroviral treatment (cART) to reduce viral burden to nearly undetectable levels in cerebrospinal fluid and serum, HIV-1 associated neurocognitive disorders (HAND) continue to persist in as many as half the patients living with this disease. There is growing consensus that the actual substrate for HAND is destruction of normal synaptic architecture but the sequence of cellular events that leads to this outcome has never been resolved. To address whether central vs. peripheral myeloid lineage cells contribute to synaptic damage during acute neuroinflammation we injected a single dose of the HIV-1 transactivator of transcription protein (Tat) or control vehicle into hippocampus of wild-type or chimeric C57Bl/6 mice genetically marked to distinguish infi

SUBMITTER: Lu SM 

PROVIDER: S-EPMC3166280 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature