Expression of HIV transgene aggravates kidney injury in diabetic mice.

Publication Type:

Journal Article


Kidney Int, Volume 83, Issue 4, p.626-34 (2013)


Albuminuria, Animals, asb, Biomarkers, Collagen Type IV, Creatinine, Diabetes Mellitus, Experimental, Diabetic Nephropathies, Disease Progression, Fibrosis, Fusion Proteins, gag-pol, Gene Expression Profiling, HIV Infections, HIV-1, Inflammation Mediators, Kidney, Mice, Mice, Inbred C57BL, Mice, Transgenic, Oligonucleotide Array Sequence Analysis, Phosphorylation, Real-Time Polymerase Chain Reaction, Reproducibility of Results, Smad3 Protein, Time Factors


With the widespread use of combination antiretroviral agents, the incidence of HIV-associated nephropathy has decreased. Currently, HIV-infected patients live much longer and often suffer from comorbidities such as diabetes mellitus. Recent epidemiological studies suggest that concurrent HIV infection and diabetes mellitus may have a synergistic effect on the incidence of chronic kidney disease. To address this, we determined whether HIV-1 transgene expression accelerates diabetic kidney injury using a diabetic HIV-1 transgenic (Tg26) murine model. Diabetes was initially induced with low-dose streptozotocin in both Tg26 and wild-type mice on a C57BL/6 background, which is resistant to classic HIV-associated nephropathy. Although diabetic nephropathy is minimally observed on the C57BL/6 background, diabetic Tg26 mice exhibited a significant increase in glomerular injury compared with nondiabetic Tg26 mice and diabetic wild-type mice. Validation of microarray gene expression analysis from isolated glomeruli showed a significant upregulation of proinflammatory pathways in diabetic Tg26 mice. Thus, our study found that expression of HIV-1 genes aggravates diabetic kidney disease.