Molecular mechanisms of infection and pathogenesis of viruses

将感染流感病毒的鸡胚尿囊膜无病毒提取物静脉注射到鸡体内，可引起血管内血液凝固而猝死。在注射肝素提取物之前静脉注射肝素的鸡存活下来，没有任何疾病迹象。结果表明，在病毒复制的组织中存在凝血因子，并对鸡表现出毒性。为了进一步了解禽鼠疫病毒的致病性，对实验感染强毒株和无毒株的鸡进行了病毒学和组织病理学比较。病毒血症后，毒性病毒在血管内皮细胞中广泛复制，而无毒病毒仅限于在呼吸道中复制。毒性病毒对血管壁造成严重损害（血管炎），导致血液异常凝固、充血、水肿和血脑屏障破裂。这些发现连同对感染组织提取物的生物学分析结果表明，血管炎介导的宿主因子引起禽鼠疫的疾病体征。

Intravenous injection into chickens with the virus-free extracts from the allantoic membrane of chicken embryos infected with influenza viruses resulted in sudden death due to blood coagulation in the vessels. The chickens injected intravenously with heparin prior to the injection with the extract survived without any signs of disease. The results suggest that some coagulation factors exist in the tissues where virus replicated and that they showed toxiciry to the chickens.To provide information on the pathogenically of fowl plague virus, virological and histopathological comparison was carried out between chickens experimentally infected with virulent and avirulent influenza virus strains. Virulent viruses replicated extensively in the vascular endothelial cells after viremia, whereas avirulent viruses were limited to replicate in the respiratory tracts. Virulent viruses induced severe damage to the vascular walls (vasculitis), leading to the abnormal coagulation of the blood as well as hyperemia, edema and breakdown of the blood-brain barrier. These findings together with the results of biological analyses on infected tissue extracts indicate that the vasculitis-mediated host factors cause the disease signs of fowl plague.