Ied [31,32]. These compounds, which include the prototypic compound NBD556 and its derivatives, mimic the effects of CD4 by inducing the exposure of the coreceptor-binding site on gp120 [31,33]. Although NBD-556 inhibits HIV-1 infection of CD4+CCR5+ cells, it can replace CD4 and thus enhance HIV-1 infection of CD42CCR5+ cells [31]. In view of their capacity to enhance infectivity, any potential ap

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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

Of plant lectins on HIV-1 transcytosis through a tight epithelial cells monolayer To evaluate the capacity of each plant lectin to inhibit in vitro HIV-1 transcytosis through genital epithelial cells, such as HEC-1A cells, we used a dual-chamber model in which the apical chamber consisted of a confluent monolayer of HEC-1A cells, and the basal chamber contained fresh medium. Cell-free virus (HIV-1

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Ir Immune Defic Syndr. Author manuscript; available in PMC 2013 June 01.Mosam et al.Pagena e, 89 had advanced (but not immediately life threatening) KS and 58 had CD4

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