Komada H, Tsurudome M, Bando H, Nishio M, Ueda M, Tsumura H, Ito Y
Department of Microbiology, Mie University School of Medicine, Japan.
J Gen Virol. 1989 Dec;70 ( Pt 12):3487-92. doi: 10.1099/0022-1317-70-12-3487.
This report describes our attempt to establish an experimental animal model for human parainfluenza virus type 4A (HPIV-4A) and 4B (HPIV-4B) infection, which was used to study the immune response to the viruses. Monkeys were inoculated intranasally with the viruses, and at 10 weeks post-infection they were re-infected with homologous subtype viruses. Virus-specific IgM and IgG serum antibodies were measured by ELISA. A small peak of IgM antibody was detected in the monkeys re-infected with HPIV-4B, whereas this response was not detected after re-infection with HPIV-4A. Virus-specific IgA and IgE antibodies were not detected in sera following infection and re-infection with HPIV-4. However virus-specific IgA and IgE antibodies were found in the saliva and nasal exudates of monkeys infected with either HPIV-4A or -4B. Re-infection of monkeys with HPIV-4B also stimulated an IgA and IgE response. To our knowledge this is the first description of an experimental animal. The kinetics of haemagglutinin-inhibition and neutralization (NT) antibodies were similar to that of virus-specific IgG antibodies. The NT titres of sera from HPIV-4A-infected monkeys were enhanced by the addition of complement, whereas complement did not affect the NT activity of sera obtained from HPIV-4B-infected animals. Antigenic specificities of IgG antibody induced by HPIV-4 infection were analysed with radioimmunoprecipitation followed by SDS-PAGE. Anti-NP, -HN and -F antibodies appeared 2 weeks after infection, and the highest titres were found 2 weeks after re-infection. Anti-F antibody production followed a biphasic pattern previously observed in mumps virus infection.
本报告描述了我们建立人4A型副流感病毒(HPIV - 4A)和4B型副流感病毒(HPIV - 4B)感染实验动物模型的尝试,该模型用于研究对这些病毒的免疫反应。将病毒经鼻内接种给猴子,在感染后10周,用同源亚型病毒再次感染它们。通过酶联免疫吸附测定法(ELISA)检测病毒特异性IgM和IgG血清抗体。在再次感染HPIV - 4B的猴子中检测到一个小的IgM抗体峰值,而再次感染HPIV - 4A后未检测到这种反应。在感染和再次感染HPIV - 4后,血清中未检测到病毒特异性IgA和IgE抗体。然而,在感染HPIV - 4A或 - 4B的猴子的唾液和鼻分泌物中发现了病毒特异性IgA和IgE抗体。用HPIV - 4B再次感染猴子也刺激了IgA和IgE反应。据我们所知,这是对实验动物的首次描述。血凝抑制和中和(NT)抗体的动力学与病毒特异性IgG抗体相似。来自HPIV - 4A感染猴子的血清的NT滴度通过添加补体而增强,而补体不影响来自HPIV - 4B感染动物的血清的NT活性。用放射免疫沉淀法继以十二烷基硫酸钠 - 聚丙烯酰胺凝胶电泳(SDS - PAGE)分析HPIV - 4感染诱导的IgG抗体的抗原特异性。抗核蛋白(NP)、血凝素 - 神经氨酸酶(HN)和融合蛋白(F)抗体在感染后2周出现,在再次感染后2周发现最高滴度。抗F抗体的产生遵循先前在腮腺炎病毒感染中观察到的双相模式。