Purpose of review: HIV-1-associated nephropathy is characterized clinically by proteinuria with azotemia and pathologically by collapsing focal segmental glomerulosclerosis with tubulointerstitial nephritis and microcystic tubular dilatation. This review summarizes the manner in which different transgenic animal models contribute to our knowledge of the pathogenesis of HIV-1-associated nephropathy.
Recent findings: The most widely studied has been a transgenic mouse model bearing a gag and pol-deleted proviral construct that develops renal disease with many of the clinical and pathologic characteristics seen in HIV-1-associated nephropathy. Studies using this model have helped to highlight the role of HIV-1 viral gene expression in renal cells, podocyte dysregulation, and genetic host factors in the pathogenesis of HIV-1-associated nephropathy. This model has provided the key insights that led to detection of HIV-1 in human kidney epithelial cells. Other transgenic models have helped define critical roles for individual HIV gene products (Nef and Vpr) in the pathogenesis of HIV-1-associated nephropathy. Transgenic mouse models have also provided a method to discover new treatments targeting various steps in the pathogenesis of this disease.
Summary: Transgenic animal models of HIV-1-associated nephropathy have contributed greatly to the progress made toward understanding the pathogenesis of this disease.