Viral infection has involved relapse of nephrotic syndrome, onset or aggravation of chronic glomerulonephritis

肾小球肾炎的病因或加重因素，如IgA肾病，仍不清楚。肾炎的发作通常是由急性病毒感染引起的，因此，我们研究了病毒感染如何参与小鼠抗gbm肾炎的恶化。雄性BALB/c小鼠静脉注射单剂量抗gbm抗体。将柯萨奇病毒B4 （CoxB4）作为肠道病毒和最小RNA病毒组，静脉注射到肾炎小鼠体内。这些小鼠被分成三组；A组于第0天静脉注射CoxB4，同时注射抗gbm抗体；B组于第7天静脉注射CoxB4，此时尿路表现恶化；C组（对照组）单独注射抗gbm抗体，无病毒攻毒。随时间测定尿蛋白排泄量及各种细胞因子。此外，这些小鼠被处死，收集肾脏进行光镜检查，免疫组织化学，并在2至14天内测量各种细胞因子的信息水平。A组尿蛋白排泄量明显高于B组和c组。这些结果表明，病毒感染对小鼠肾炎的病程有影响，尤其是早期感染。

The etiology or aggravation factors of glomerulonephritis, such as IgA nephropathy, is still unclear. Episodes of nephritis are frequently proceeded by acute viral infections, therefore, we examined how viral infection would be participating in the exacerbation of anti-GBM nephritis in mice.Male BALB/c mice were injected intravenously with a single dose of anti-GBM antibody. Coxsackievirus B4 (CoxB4), in the group of enterovirus and minimum RNA virus, was inoculated intravenously into the nephritis induced mice. These mice were divided into three groups ; in group A, CoxB4 was injected intravenously on day 0, simultaneously with anti-GBM antibody injection, : in group B, CoxB4 was injected intravenously on day 7, when urinary findings worsening, : in group C (control group), anti-GBM antibody was alone injected, no challenged with virus. The amount of urine protein excretion and various cytokines were measured with time. Moreover, these mice were sacrificed, and the kidneys were collected for light microscopy, immunohistochemistory, and measurements of the message levels of various cytokines from 2 to 14 days.The amounts of urinary protein excretion were significantly increased in group A, than group B or group C.These results indicate that the course of nephritis in mice was influenced by viral infections, especially on early stage infections.