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缺陷干扰病毒对三株小鼠在体内的致死性流感的保护作用。

Protection of three strains of mice against lethal influenza in vivo by defective interfering virus.

作者信息

Morgan D J, McLain L, Dimmock N J

机构信息

Department of Biological Sciences, University of Warwick, Coventry, UK.

出版信息

Virus Res. 1993 Aug;29(2):179-83. doi: 10.1016/0168-1702(93)90058-u.

DOI:10.1016/0168-1702(93)90058-u
PMID:8212859
Abstract

This report examines the protective effects of defective interfering (DI) WSN on three strains of mice (C3H/He-mg (H-2k), C57BL/6 (H-2b) and BALB/c (H-2d)) infected with various doses of A/WSN influenza virus. All three strains were protected in terms of morbidity and mortality, to varying extents, DI WSN protected optimally against a low but lethal dose of A/WSN in C3H/He-mg mice, but also protected this and other strains against very high doses of A/WSN. Intermediate sized inocula gave little, if any, protection. In all cases protection required an active DI genome since inactivation with beta-propiolactone abrogated any sparing effect. Consolidation of the lungs was reduced by treatment with active DI virus, but at some doses of inoculum there was reduction in lung pathology without reduction of mortality. Treatment of infected mice with DI virus did not reduce the lung virus titre, but in C3H/He-mg mice resulted in recovery of infectious virus from other tissues, notably the heart, where it was not normally found. No infectivity was recovered from brain, liver or serum. Haemagglutination-inhibiting (HI) antibody could not be detected in the lungs of any of the infected mice co-inoculated with the control BPL-inactivated DI WSN but was present in considerable amounts in all three strains when these were co-inoculated with DI virus. These and previous data (Morgan and Dimmock, 1992) suggested that influenza virus was immunosuppressive and that active DI virus abrogated these suppressive effects.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本报告研究了缺陷干扰(DI)WSN对感染不同剂量A/WSN流感病毒的三种小鼠品系(C3H/He-mg(H-2k)、C57BL/6(H-2b)和BALB/c(H-2d))的保护作用。在发病率和死亡率方面,所有三个品系均得到了不同程度的保护。DI WSN对C3H/He-mg小鼠中低剂量但致死剂量的A/WSN提供了最佳保护,同时也保护了该品系及其他品系免受高剂量A/WSN的侵害。中等剂量接种几乎没有提供保护作用。在所有情况下,保护作用都需要活性DI基因组,因为用β-丙内酯灭活会消除任何保护作用。活性DI病毒治疗可减轻肺部实变,但在某些接种剂量下,肺部病变减轻但死亡率并未降低。用DI病毒治疗感染小鼠并没有降低肺部病毒滴度,但在C3H/He-mg小鼠中,导致从其他组织(尤其是心脏,通常在此处未发现传染性病毒)中恢复了传染性病毒。在脑、肝或血清中未检测到传染性。在与对照BPL灭活的DI WSN共同接种的任何感染小鼠的肺部中均未检测到血凝抑制(HI)抗体,但当与DI病毒共同接种时,所有三个品系中均存在大量HI抗体。这些数据和之前的数据(Morgan和Dimmock,1992)表明,流感病毒具有免疫抑制作用,而活性DI病毒可消除这些抑制作用。(摘要截取自250字)

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