[Experimental glomerulonephritis induced by Coxsackie B4 virus in mice--glomerular changes associated with intermittent viral inoculations].

It has been considered that viruses may be implicated in the genesis and progression of glomerular diseases. Several experimental and clinical studies have reported nephritogenecity of Coxsackie (Cox.) B4 virus infection. So in order to elucidate glomerulopathy of intermittent Cox. B4 virus infection, one-month-old Swiss albino mice were inoculated intravenously with purified Cox. B4 virus, 3 x 10(7) TCD50, once a month, and then were sacrificed from 4 to 9 mo. of age (from 3 to 8 times inoculation) at one month after final inoculation. Virological assay of neutralization titer (NT) of sera and histological study of the kidneys were performed. The results were as follows: 1) NT of sera was 1:16 at 4 mo. of age and gradually elevated to 1:256 at 8 and 9 mo. of age. 2) Light microscopy revealed PAS-positive mesangial deposits that were increased by degrees and marked showing hemispherically. Several glomeruli had GBM alteration, mesangial sclerosis and crescent formation with interstitial inflammatory response. 3) By immunofluorescence, IgG, IgA, and Cox. B4 viral antigen were stained in mesangial pattern and its intensity were increased in proportion to the number of inoculations. These results demonstrated that intermittent intravenous inoculation with Cox. B4 virus in mice produces virus mediated immune complex type glomerulonephritis closely resembling those in human chronic glomerulonephritis with mesangial immune deposits.