Highly Pathogenic H5N1 Influenza Virus Infection in Migratory Birds

严重急性呼吸综合征是一种新近出现的严重传染性疾病,病原体为一种新的冠状病毒。但其免疫病理的发病机制尚未阐明,我们用SARS病毒感染了恒河猴和leiws大鼠,经PCR和抗体检测,证明病毒在动物体内有复制。用酶连免疫吸附试验测量动物血清中白介素(IL)-6,白介素(IL)-10,γ-干扰素(INF),肿瘤坏死因子(TNF)-α的含量。结果显示,血清中IL-10和INF-γ的含量在感染前后无显著性差异。感染后动物体内IL-6显著升高,其含量与肺部病变程度呈正相关。TNF-α的含量降低。动物模型中血清免疫因子的测定避免了临床病人由于使用抗病毒药物和激素造成的干扰,对于我们了解免疫因子在SARS免疫病理发病机制的作用有一定帮助。

Plasma Inflammatory Cytokines inSevere Acute Respiratory Syndrome Animal Model

To understand the mechanisms of H5N1 pathogenicity, we infected 6 to 8-week-old BALB/c mice by different routes of viral inoculation. The virus caused severe disease in mice, characterized by induced hypothermia, rapid weight loss, and high mortality by 2 days postinfection. And the main clinical signs of the animals began to recover by 4 days postinfection. The most severe and widespread lesions were observed in the organs of virus-infected mice, where received the virus firstly. Only mild lesions or no lesions were observed in spleens and brains. The principal lesions were occured in 2 days postinfection. Except kidney and heart, the lesions were recovered after 4 days postinfection.