Bassel E. Sawaya

TL;DR: It is demonstrated that neurons can take up Vpr that is released into the supernatant of HIV-infected microglia, and the permeability of the plasma membrane increases in neurons treated with Vpr, concluding that soluble Vpr is a major viral factor that causes a disturbance in neuronal communication leading to neuronal dysfunction.

TL;DR: It is concluded that instead of causing cell death, low concentration of HIV‐1 Vpr altered neuronal function related with inhibition of mitochondria axonal transport which might contribute to the accelerated neuronal aging.

TL;DR: The results showed that expression of TCF-4 in human astrocytic cells (U-87MG cells) decreased the basal and Tat-mediated transcription of the HIV-1 long terminal repeat (LTR), providing evidence for the cooperative interaction of TCf-4, the important transcription factor of the Wnt pathway, with Tat; this interaction may determine the level of viral gene transcription inhuman astroCytic cells.

TL;DR: The results indicate that Tat production causes a noticeable increase in the survival rate of PC12 cells upon their treatment with genotoxic agents, ascribing a new role for Tat in host genomic integrity, perhaps by affecting the expression of genes involved in DNA repair.

TL;DR: Evidence is presented that the GRS gel shift seen on cellular stimulation is due to Egr-1, and that TPA-induced G RS gel shift could be blocked by antibody to EGr-1.