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由免疫原性高和低的流感病毒株引起的流感感染的特点。

Peculiarities of influenza infection caused by highly and poorly immunogenic strains of influenza virus.

作者信息

Frolov A F, Skripchenko G S, Shcherbinskaya A M, Vlasova A G, Rybakova T M

出版信息

J Hyg Epidemiol Microbiol Immunol. 1984;29(3):303-9.

PMID:6544322
Abstract

The authors studied the peculiarities of the course of experimental influenza infection induced by the administration of highly and poorly immunogenic strains of influenza virus to mice. Influenza viruses with varying immunogenic activity were obtained from the vaccine strain A/Victoria/35/72/50 (H3N2) by immunoselection modelling the process of natural selection. The administration of strains with high and poor immunogenicity to mice of the F1 (CBA X C57B1) line led to the development of acute influenza infection accompanied by reproduction of viruses in the tissue of the lungs and other internal organs. The poorly immunogenic strain 5/II-Victoria, unlike the initial virus A/Victoria/35 and its highly immunogenic variant 2/I-Victoria, is able to circulate for a long time in the organism of the infected animal causing development of chronic inflammatory processes and stimulating the formation of neoplasms. Immunogenicity is thus one of the factors determining the character of the course of experimental influenza infection. A conclusion was drawn concerning the epidemiological and aetiological importance of viruses with reduced immunogenicity and their role in the evolution of influenza virus. It is presumed that reduced immunogenicity is one of the adaptation mechanisms of aggression permitting the population of influenza virus to escape control by specific humoral immunity.

摘要

作者研究了给小鼠接种高免疫原性和低免疫原性流感病毒株所引发的实验性流感感染病程的特点。通过免疫选择模拟自然选择过程,从疫苗株A/维多利亚/35/72/50(H3N2)获得了具有不同免疫原活性的流感病毒。给F1(CBA×C57B1)品系的小鼠接种高免疫原性和低免疫原性毒株,导致急性流感感染的发生,同时病毒在肺组织和其他内脏器官中复制。与初始病毒A/维多利亚/35及其高免疫原性变体2/I - 维多利亚不同,低免疫原性毒株5/II - 维多利亚能够在受感染动物体内长时间循环,引发慢性炎症过程并刺激肿瘤形成。因此,免疫原性是决定实验性流感感染病程特征的因素之一。得出了关于免疫原性降低的病毒的流行病学和病因学重要性及其在流感病毒进化中的作用的结论。据推测,免疫原性降低是侵袭的一种适应机制,使流感病毒群体能够逃避特异性体液免疫的控制。

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