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

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

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Erapy, and had received methadone or buprenorphine for 3 weeks at the OTP with no plans to discontinue. We also required verbal approval from participants' HIV providers and confirmation of active insurance coverage for ART. Exclusion criteria included ART dosed more frequently than twice daily, use of liquid medication, and use of a regimen that was predicted to have fewer than 1.5 active drugs

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Er. Cells were incubated for 1 h at 37 . HIV-1 transcytosis was assessed by detecting the presence of p24 antigen (HIV-1 core profile ELISA) in the basolateral chamber of the transwell. The inhibition of transcytosis was expressed as the percentage of p24 antigen recovered in the basolateral chamber in the presence of each plant lectin by comparison to that recovered without the plant lectins. HIV

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