title: HIV-1 Vpr activates the DNA damage response in renal tubule epithelial cells.
abstract: HIV-associated nephropathy (HIVAN) is a major cause of HIV-related morbidity and mortality. Pathogenesis involves direct infection of the glomerular and tubular epithelial cells leading to characteristic disorder. Recently, we have shown that HIV-1 Vpr causes hypertrophy, hyperploidy, and apoptosis. Here, we report that Vpr activates the DNA damage response resulting in the observed renal phenotype. Renal sections from the HIVAN transgenic mouse model and human biopsies both show an abundant DNA damage response.
authors: Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA.
authors: Paul E
authors: PE
authors: Rosenstiel
authors: Justin
authors: J
authors: Chan
authors: Alexander
authors: A
authors: Snyder
authors: Vicente
authors: V
authors: Planelles
authors: Vivette D
authors: VD
authors: D'Agati
authors: Paul E
authors: PE
authors: Klotman
authors: Mary E
authors: ME
authors: Klotman
mesh_terms: D016263:AIDS-Associated Nephropathy / Q000473:pathology*; D000818:Animals; D002460:Cell Line; D004249:DNA Damage; D004279:DNA, Viral / Q000032:analysis; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000187:drug effects / Q000821:virology; D016336:Gene Products, vpr / Q000494:pharmacology*; D015497:HIV-1 / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D007684:Kidney Tubules / Q000187:drug effects / Q000821:virology; D051379:Mice; D008822:Mice, Transgenic
chemical_list: D004279:DNA, Viral; D016336:Gene Products, vpr