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Simian-human immunodeficiency virus-associated nephropathy in macaques.
E B Stephens1, C Tian, S B Dalton
1Department of Microbiology, Molecular Genetics, and Immunology, University of Kansas Medical Center, Kansas City 66160, USA. estephen@kumc.edu
AIDS Research and Human Retroviruses
|August 25, 2000
Summary
Researchers developed pathogenic simian-human immunodeficiency virus (SHIV) strains to study AIDS-related kidney disease. SHIV-KU-2MC4 causes severe glomerular pathology in macaques, offering a model for studying glomerulosclerosis.
Area of Science:
- Virology
- Pathology
- Immunodeficiency Viruses
Background:
- Chimeric simian-human immunodeficiency virus (SHIV) strains were created using HIV-1 and SIV(mac)239 components.
- These SHIV strains were derived from a nonpathogenic parental virus, SHIV-4.
Purpose of the Study:
- To investigate the renal pathology associated with the development of pathogenic SHIV strains.
- To establish a model for studying SHIV-associated glomerulosclerosis.
Main Methods:
- Derivation of pathogenic SHIV strains from SHIV-4.
- Inoculation of macaques (pigtail and rhesus) with derived SHIV strains.
- Analysis of renal pathology, CD4+ T cell counts, and clinical signs.
Main Results:
- SHIV-KU-1 caused rapid CD4+ T cell loss but limited renal pathology in pigtail macaques.
- SHIV-KU-2 induced renal pathology in rhesus macaques, affecting <10% of glomeruli.
- SHIV-KU-2MC4 caused significant neurologic and renal pathology, with >60% of glomeruli involved and uremic BUN levels.
Conclusions:
- SHIV-KU-2MC4 induces severe glomerular pathology in rhesus macaques.
- This model is suitable for analyzing molecular determinants of SHIV-associated glomerulosclerosis.