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Experimental IgA nephropathy induced by coxsackie B4 virus in mice
Abstract:
Viruses have been suspected to be etiological agents of IgA nephropathy. Recently, viruses were detected in renal tissues from patients with IgA nephropathy. We tried to cause lesions similar to IgA nephropathy by inoculating virus into mice and to detect virus RNA in the lesion by in situ hybridization. A group of mice were inoculated intravenously with coxsackie B4 virus once a month from 1 to 5 months of age and sacrificed monthly from 6 to 12 months of age. Mesangial proliferation and deposits that stained positive with periodic acid-Schiff in light microscopy and electron-dense deposits in electron microscopy were found from 6 months of age. Positive findings for IgG and IgA deposition in the mesangium were noted and the intensity of IgA deposition was predominant after 10 months of age. The signals of coxsackie B4 virus by in situ hybridization were observed in the lesions. These observations indicate that coxsackie B4 virus inoculated repeatedly into mice induces lesions similar to IgA nephropathy. The depositions of the lesions may be immune complexes of coxsackie B4 virus and these immune complexes injure renal tissues.
Insights
Coxsackie B4 virus can cause IgA nephropathy-like kidney lesions in mice. Viral RNA was detected in these lesions, suggesting a viral role in the disease.
Area of Science:
- Nephrology
- Virology
- Immunology
Background:
- IgA nephropathy (IgAN) is a kidney disease where immune deposits, primarily IgA, accumulate in the glomeruli.
- Viruses have been implicated as potential triggers for IgAN, with viral detection in renal biopsies of affected patients.
Purpose of the Study:
- To investigate the potential etiological role of viruses in IgA nephropathy.
- To establish an animal model of IgAN using coxsackie B4 virus.
Main Methods:
- Intravenous inoculation of coxsackie B4 virus into mice monthly from 1 to 5 months of age.
- Histopathological examination (light and electron microscopy) and in situ hybridization for viral RNA detection at monthly intervals from 6 to 12 months of age.
Main Results:
- Mice developed mesangial proliferation and characteristic deposits (PAS-positive, electron-dense) starting at 6 months.
- IgG and IgA deposition in the mesangium was observed, with predominant IgA after 10 months.
- Coxsackie B4 virus RNA signals were detected within the renal lesions.
Conclusions:
- Repeated coxsackie B4 virus inoculation in mice induces renal lesions resembling human IgA nephropathy.
- Deposited immune complexes, potentially involving coxsackie B4 virus, are implicated in the renal tissue injury observed in this model.