Open AccessHIV-1 Vpr activates the DNA damage response in renal tubule epithelial cells
Author(s) -
Philip Rosenstiel,
Justin Chan,
Alexander Snyder,
Vicente Planelles,
Vivette D. D’Agati,
Paul E. Klotman,
Mary E. Klotman
Publication year - 2009
Publication title -
aids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.195
H-Index - 216
eISSN - 1473-5571
pISSN - 0269-9370
DOI - 10.1097/qad.0b013e32833088a0
Subject(s) - pathogenesis , apoptosis , dna damage , nephropathy , phenotype , biology , transgene , genetically modified mouse , kidney , human immunodeficiency virus (hiv) , dna , cancer research , virology , microbiology and biotechnology , immunology , gene , genetics , endocrinology , diabetes mellitus
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.