Larson C H
Am J Vet Res. 1976 Jul;37(7):823-30.
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.
本研究旨在通过腹腔注射亚致死剂量的鼠巨细胞病毒,对实验室小鼠诱发的肾小球肾炎的临床和超微结构方面进行研究并建立关联。试图确定肾小球变化的发病机制以及由此产生的病毒血症。鼠巨细胞病毒感染在HA/ICR品系的年轻雌性小鼠中引起急性短暂性肾小球肾炎。经亚致死剂量的匀浆感染性腺接种后存活的小鼠出现短暂性蛋白尿,并排出肾小管管型。鼠巨细胞病毒感染导致了一种对系膜细胞具有选择性的肾小球病变。病毒通过吞噬作用进入系膜细胞后,在细胞核中复制,并排泄到系膜基质通道中,向毛细血管袢周边延伸并靠近尿腔。感染后第5天肾小球中很少发现病毒颗粒,且未观察到慢性肾脏疾病。