Astry C L, Yolken R H, Jakab G J
J Med Virol. 1984;14(2):81-90. doi: 10.1002/jmv.1890140202.
Mice were infected by aerosol inhalation with influenza A/PR8/34 virus, and the kinetics of infection were monitored by the measurement of infectious virus, viral neuraminidase activity, and viral antigen as detected by enzyme immunoassay. Pulmonary levels of neuraminidase activity closely paralleled the infectious titers quantitated by standard egg inoculation techniques. Both viral neuraminidase activity and viral antigen increased in a dose-dependent manner during the early stages of the viral infection. After day 5, however, viral neuraminidase activity precipitously declined, whereas viral antigen levels remained elevated at high concentration for up to 60 days. Immunosuppressive treatment with cyclophosphamide resulted in the prolonged maintenance of peak virus titers without any additional increases in viral antigen. Previously infected mice were resistant to reinfection with homologous virus as evidenced by the lack of detectable viral neuraminidase activity and the lack of generation of additional viral antigen. These data define the temporal relationship between levels of infectious virus, neuraminidase activity, and viral antigen in an experimental model of influenza virus infection.
通过气溶胶吸入法用甲型流感病毒A/PR8/34感染小鼠，并通过测量感染性病毒、病毒神经氨酸酶活性以及酶免疫测定法检测的病毒抗原，来监测感染的动力学。肺部神经氨酸酶活性水平与通过标准鸡胚接种技术定量的感染滴度密切平行。在病毒感染的早期阶段，病毒神经氨酸酶活性和病毒抗原均呈剂量依赖性增加。然而，在第5天后，病毒神经氨酸酶活性急剧下降，而病毒抗原水平在高浓度下持续升高长达60天。用环磷酰胺进行免疫抑制治疗导致病毒滴度峰值的持续维持，而病毒抗原没有任何额外增加。先前感染的小鼠对同源病毒的再感染具有抵抗力，这表现为缺乏可检测到的病毒神经氨酸酶活性以及没有额外病毒抗原的产生。这些数据确定了流感病毒感染实验模型中感染性病毒水平、神经氨酸酶活性和病毒抗原之间的时间关系。
