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实验性呼吸道合胞病毒感染诱导BALB/c小鼠产生的局部和全身免疫反应分析。

Analysis of the local and systemic immune responses induced in BALB/c mice by experimental respiratory syncytial virus infection.

作者信息

Anderson J J, Norden J, Saunders D, Toms G L, Scott R

机构信息

Department of Virology, School of Pathological Sciences, Medical School, University of Newcastle upon Tyne, U.K.

出版信息

J Gen Virol. 1990 Jul;71 ( Pt 7):1561-70. doi: 10.1099/0022-1317-71-7-1561.

DOI:10.1099/0022-1317-71-7-1561
PMID:2197371
Abstract

Pulmonary A2 strain respiratory syncytial virus infection of BALB/c laboratory mice persisted for up to 7 days after initial infection with peak virus titres being recovered on day 4. Virus antigen within the lungs was found to be restricted essentially to the alveolar regions. Similarly, pulmonary histopathological changes remained confined to the peri-alveolar regions being consistent with mild pneumonia. Infection was found to elicit a pulmonary major histocompatibility complex-restricted cytotoxic T lymphocyte (CTL) response which was first detectable 6 days after infection and optimal 7 to 9 days after infection. This local CTL response was preceded by a rapid transient virus-specific lymphocyte transformation response which was detectable only 3 days after intranasal infection. In addition, infection induced rapid interferon production within the lungs which was accompanied by an equally rapid rise in pulmonary natural killer (NK) cell cytotoxic activity. Enhanced NK cell cytotoxicity could be detected after only 1 day post-infection and continued to rise to maximum levels on day 3. This response like the acute CTL response was found to be restricted to the lower respiratory tract. IgG was the first class of virus-specific immunoglobulin to be detected in the lungs of infected animals after experimental infection. However, IgG was not detected until day 10 post-infection, 5 days after the initial decline of virus shedding. Virus-specific IgA although detectable did not appear in the lung until day 24.

摘要

BALB/c实验小鼠感染A2株呼吸道合胞病毒后,在初次感染后可持续长达7天,病毒滴度在第4天达到峰值。肺内病毒抗原主要局限于肺泡区域。同样,肺部组织病理学变化也局限于肺泡周围区域,与轻度肺炎一致。研究发现,感染会引发肺部主要组织相容性复合体限制的细胞毒性T淋巴细胞(CTL)反应,感染后6天首次可检测到,感染后7至9天达到最佳状态。这种局部CTL反应之前是快速短暂的病毒特异性淋巴细胞转化反应,仅在鼻内感染后3天可检测到。此外,感染会在肺内迅速诱导干扰素产生,同时肺内自然杀伤(NK)细胞细胞毒性活性也会同样迅速升高。感染后仅1天即可检测到NK细胞细胞毒性增强,并在第3天持续上升至最高水平。发现这种反应与急性CTL反应一样,局限于下呼吸道。IgG是实验感染后在感染动物肺中检测到的第一类病毒特异性免疫球蛋白。然而,直到感染后第10天,即病毒排出量首次下降5天后,才检测到IgG。病毒特异性IgA虽然可检测到,但直到第24天才出现在肺中。

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