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Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models
Published on: December 3, 2019
Glomerular MYH9 expression is reduced by HIV-1
Thomas Hays1, Vivette D D'Agati, Jonathan A Garellek
1Mount Sinai School of Medicine, Department of Medicine, New York, New York, USA. thomas.hays@mssm.edu
AIDS (London, England)
|February 9, 2012
Summary
HIV-associated nephropathy (HIVAN) involves reduced MYH9 gene expression in kidney podocytes. This down-regulation by HIV-1 may contribute to HIVAN development and progression.
Area of Science:
- Nephrology
- Virology
- Molecular Biology
Background:
- HIV-associated nephropathy (HIVAN) presents a significant disease burden.
- Understanding HIVAN pathogenesis requires investigating molecular mechanisms.
- MYH9 gene mutations cause Mendelian renal disease, suggesting its importance in kidney function.
Purpose of the Study:
- To investigate the hypothesis that HIV-1 down-regulates renal MYH9 expression in HIVAN.
- To determine the role of MYH9 in the pathogenesis of HIVAN.
Main Methods:
- Immunofluorescence to assess glomerular MYH9 expression in HIV-1 transgenic mice.
- Analysis of Myh9 expression in HIV-1 transgenic and human podocytes.
- Quantitative assessment of MYH9 protein and message levels in human podocytes and glomeruli.
Main Results:
- Glomerular MYH9 expression was reduced in HIV-1 transgenic mice.
- HIV-1 transgenic podocytes showed reduced Myh9 expression at the protein level.
- Human podocytes transduced with HIV-1 exhibited significantly reduced MYH9 at both protein and message levels.
- MYH9 is highly expressed in human glomeruli and podocytes, with significant reduction observed in HIVAN cases.
Conclusions:
- The podocyte response to HIV-1 involves down-regulation of MYH9 expression.
- Reduced MYH9 expression is hypothesized to play a role in HIVAN pathogenesis.
