Coproteins [1]. Binding of gp120 to the receptor, CD4, on the target cell surface induces major conformational changes in the envelope glycoproteins [2]. These changes allow gp120 to bind the viral coreceptor, either CXCR4 or CCR5 [3?]. CD4 binding also induces the formation of a gp41 pre-hairpin intermediate, in which three hydrophobic grooves on the surface of a coiled coil formed by the heptad

Ignificantly longer lives. While HAART has been increasing the lifespan of those infected with HIV, it has also led to an increased prevalence of HAD [32-38]. As the pathology of HAD, like Alzheimer's Disease (AD), is commonly characterized by an increase in the amount of amyloid-beta (Ab) peptide in the brain [39], evidence suggesting microglia modulate the clearance of potentially neurotoxic Ab

Owed a direct correlation between microglial activation/infection and cognitive decline [19]. Studies have found microglial HIV infection as central in exacerbating HIV dementia [20,21]. Importantly, neuronal dysfunction and death in HIV infection results from cytokine stimulation, but especially several cytokine-mediated apoptotic mechanisms emanating from microglia. Thus microglial cytokine prod

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Y and also visibly damaged subcortical areas [45,46]. Amyloid plaques in AD result from the deposition of amyloid beta (Ab) which is a putative pathogenic molecule in AD. Ab is the cleavage product of the amyloid precursor protein (APP) and APP mutations are associated with inherited forms of AD. The clinical implication or pathogenic consequences of brain amyloid deposition are still controversia

Ents/the study: MCL MAM KKH TCG SA DCP GT GS JS DMM BFH. Analyzed the data: MAM KKH DJM JDA TCG SA BBH DCP MC GT PAG HXL BFH. Collected data/did experiments for the study: MCL MAM KKH DJM JFW JDA TCG SA BBH NAV SP DCP MC GT GS JE NJS CBH HXL MM GHK BFH. Enrolled patients: MC PAG GS JE CBH MM DMM. Wrote the first draft of the paper: MCL BFH. Contributed to the writing of the paper: MCL MAM BBH NAV

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