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Updated: Aug 16, 2026
Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates
Published on: July 6, 2013
Murine cytomegalovirus glomerulonephritis: clinical and ultrastructural observations
Abstract:
This investigation was initiated to study and correlate the clinical and ultrastructural aspects of glomerulonephritis induced in the laboratory mouse by the intraperitoneal injection of a sublethal dose of murine cytomegalovirus. An attempt was made to ascertain the pathogenesis of the glomerular changes and the resultant viremia. Murine cytomegalovirus infection caused an acute transient glomerulonephritis in young female mice of the HA/ICR strain. Mice that survived a sublethal inoculation of homogenized infected gland developed transient proteinuria and excreted tubular casts. The murine cytomegalovirus infection resulted in a glomerular lesion that was selective for the mesangial cell. After entering the mesangial cell by phagocytosis the virus replicated in the nucleus and was excreted into the channel of the mesangial matrix, with extension toward the periphery of the capillary loop and adjacent to the urinary space. Virus particles were rarely found in the glomerulus after the 5th day of infection and chronic renal disease was not observed.
Insights
Murine cytomegalovirus (CMV) infection causes acute, temporary glomerulonephritis in mice, targeting mesangial cells. The study found no evidence of chronic kidney disease following this transient viral infection.
Area of Science:
- Nephrology
- Virology
- Immunology
Background:
- Glomerulonephritis is a significant kidney disease.
- Viral infections can impact renal function.
- Understanding viral pathogenesis in the kidney is crucial.
Purpose of the Study:
- To investigate the clinical and ultrastructural effects of murine cytomegalovirus (CMV) on the glomerulus.
- To determine the pathogenesis of CMV-induced glomerular injury and viremia.
- To assess the potential for chronic renal disease following CMV infection.
Main Methods:
- Induction of glomerulonephritis in laboratory mice via intraperitoneal injection of sublethal murine CMV.
- Clinical observation for proteinuria and tubular casts.
- Ultrastructural analysis of glomerular lesions.
- Monitoring for virus presence in renal tissue.
Main Results:
- Murine CMV infection induced acute, transient glomerulonephritis in young female HA/ICR mice.
- Surviving mice exhibited temporary proteinuria and excreted tubular casts.
- The primary glomerular lesion targeted mesangial cells, with viral replication observed within these cells.
- Virus particles were cleared from glomeruli by day 5, and no chronic renal disease developed.
Conclusions:
- Murine CMV causes a selective, acute mesangial cell injury.
- The infection is transient, with no long-term renal damage observed.
- This model provides insight into viral-induced glomerulonephritis and its resolution.
