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甲型/鸡/宾夕法尼亚/1/83病毒对鸡的致死性流感病毒感染的保护作用:保护效果的特征分析

Protection of chickens from lethal influenza virus infection by influenza A/chicken/Pennsylvania/1/83 virus: characterization of the protective effect.

作者信息

Chambers T M, Webster R G

机构信息

Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38101.

出版信息

Virology. 1991 Jul;183(1):427-32. doi: 10.1016/0042-6822(91)90160-d.

Abstract

The influenza A/chicken/Pennsylvania/1/83 (H5N2) virus is the first known example of an influenza virus isolated from a natural infection which contained primarily defective interfering particles (T. M. Chambers and R. G. Webster, J. Virol. 61, 1517-1523, 1987). In chickens, coinoculation of this virus together with the closely related but highly virulent influenza A/chicken/Pennsylvania/1370/83 virus results in reduced mortality compared to virulent virus infection alone (Bean et al., J. Virol. 54, 151-160, 1985). The biological basis of this protective effect has not been established. Protective activity required greater than or equal to 100-fold excess input of protecting virus over virulent virus, functioned effectively during the first generations of virulent virus multiplication, and also functioned against an antigenically heterologous (H7N7) virulent influenza virus. Protection was correlated with the complete inhibition of virulent virus spread to the brain of infected chickens. Plaque-purified chicken/Pennsylvania/1/83 virus depleted of defective interfering particles, and beta-propiolactone-inactivated virus, had no protective effect. These characteristics are consistent with the hypothesis that protection was the result of defective interfering particle-mediated interference with virulent virus multiplication within the respiratory tract of the chicken.

摘要

甲型流感病毒/鸡/宾夕法尼亚/1/83(H5N2)是从自然感染中分离出的首例已知流感病毒,其主要包含缺陷干扰颗粒(T.M.钱伯斯和R.G.韦伯斯特,《病毒学杂志》61卷,1517 - 1523页,1987年)。在鸡中,将这种病毒与密切相关但高致病性的甲型流感病毒/鸡/宾夕法尼亚/1370/83一起接种,与单独感染强毒病毒相比,死亡率降低(比恩等人,《病毒学杂志》54卷,151 - 160页,1985年)。这种保护作用的生物学基础尚未明确。保护活性需要保护病毒的输入量比强毒病毒高出大于或等于100倍,在强毒病毒增殖的第一代期间有效发挥作用,并且对抗原性异源的(H7N7)强毒流感病毒也有效。保护作用与强毒病毒向感染鸡大脑的传播被完全抑制相关。去除缺陷干扰颗粒的空斑纯化鸡/宾夕法尼亚/1/83病毒以及经β-丙内酯灭活的病毒没有保护作用。这些特征与以下假设一致,即保护作用是缺陷干扰颗粒介导的对鸡呼吸道内强毒病毒增殖的干扰的结果。

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