Figure 1: Molecular mechanisms of HIV-induced oxidative stress. Nef, Vpr and Tat proteins have been described as direct modulators of oxidative stress by: interaction between Nef and HcK (hemopoietic cell kinase)promoting phosphorylation of p47-phox (1), Nef-induced actin polymerization via Rac/PAK pathway (3); Vpr-induced oxiphosphatidylcholine (OxPC) in response to oxidative stress (5) and, association to ANT (adenine nucleotide translocator) contributing to mitochondrial dysfunction; diminished SOD synthesis and intracellular glutathione (GSH) via Tat (6).