Korean Journal of Nephrology 1994;13(1):62-76.

신증후성출혈열 환자의 신생검조직에서 단클론항체를 사용한 한탄바이러스 항원의 증명

채동완 , 강응택 , 안규리 , 한진석 , 김성권 , 이정상 , 김용일

Abstract

Of the various clinical syndromes of viral hemorr- hagic fever acute renal failure (ARF) is unique clinical syndrome to hemorrgagic fever with renal syndrome (HFRS). Although the clinical features and renal pathol- ogy of ARF in Korean hemorrhagic fever (KHF), one of HFRS, are well known its pathogenesis is still unclear. Hence we attempted to localize envelope glycoprotein of Hantaan virus in biopsies from patients from Korean hemorrhagic fever as a evidence of direct viral invasion of renal tissue by Hantaan virus. We studied sequential sections of kidney biopsy specimens from 23 serological- ly confirmed patients with Korean hemorrhagic fever diagnosed between June 1985 and December 1989 in Seoul National University Hospital. The sections were stained by avidin-biotinperoxidase complex method using monoclonal antibodies to Gl and G2 envelope glycoproteins. The results obyained are as follows. 1) The viral envelope glycoproteins were detected in 22 of 23 patients. 2) In all 22 patients the viral glycoprotein were localized in perinuclear cytoplasm of tubular epithelial cells in coarse granular pattern and the distribution of glyco- proteins were focal. 3) In 16 patients the viral glycoprotein were localized in the sloughed tubular epithelial cells, where tubular degenerative changes were prominent. 4) Although less strong in intensity than in tubular epithelial cells viral glycoproteins were also observed in interstitial capillary (10 cases), interstitial infiltrating cells (11 cases), glomerular mesangium (3 cases), and glomerular capillary (9 cases). 5) There were no correlations between intensity and/ or distributions of viral envelope glycorpotein and vari- ous clinical findings such as the presence duration of oliguria, maximurn diuretic urine volume. 6) At light microscopic examination major findings were shown in tubule and interstitium. On the contray there were no significant findings in vessele and glomeruli except mild mesangial expansion in 12 cases and vascular endothelial hyperplasia in 2 cases. Mild mesangial deposition of C3 and/or immunoglobulin was observed in 12 cases and only 1 case showed tubular deposition of C3 and these immunofluorescent findings were not related to intensity and/or distribution of viral envelope glycoprotein. From the above findings we could see that Hantaan viral envelope glycoproteins were localized in tubular epithelial cells with concomittant major pathologic changes but without significant immunoglobulin or complement depositions. Hence direct viral invasion may play some role in the pathogenesis of ARF in KHF.