Human immunodeficiency virus viral protein R as an extracellular protein in neuropathogenesis.

摘要: Numerous studies published in the past two decades have identified viral protein R (Vpr) as one of most versatile proteins life cycle human immunodeficiency virus type 1 (HIV-1). In this regard, more than a thousand Vpr molecules are present extracellular particles. Subsequent to entry, participates early replicative events by assisting genome nuclear import and, during cycle, shuttling between nucleus and cytoplasm accomplish its functions within context other functions. Additionally, several implicated proapoptotic because it promotes formation permeability transition pores mitochondria, which turn affects transmembrane potential adenosine triphosphate synthesis. Recent virion-free serum cerebrospinal fluid patients infected with HIV-1 whose plasma viremia directly correlates concentration Vpr. These observations pointed new role for an additional weapon arsenal, involving use target possibly inhibit HIV-1-uninfected bystander cells enable them escape immune surveillance. addition, decreases levels intracellular redox balance neurons, ultimately causing their apoptosis. Herein, we review downstream effects on cellular metabolism, functionality, survival, particular emphasis how Vpr-induced oxidative stress might aggravate HIV-1-induced symptoms, thus affecting pathogenesis disease progression.