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首页> 外文期刊>Acta Virologica: International Journal >In vitro growth profiles of respiratory syncytial virus in the presence of influenza virus.
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In vitro growth profiles of respiratory syncytial virus in the presence of influenza virus.

机译:存在流感病毒时呼吸道合胞病毒的体外生长情况。

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摘要

To elucidate epidemiological interference between respiratory syncytial (RSV) and influenza viruses, the influence of influenza A (HlN1) virus on the growth of RSV was examined. Although RSV grew in MDCK cells, coinfection with influenza A virus led to a reduction of progeny RSV. The degree of growth interference depended on the time of infection with influenza A virus post infection (p.i.) with RSV. In fact, infection with influenza A virus 12 hrs p.i. with RSV did not influence growth of the latter virus. On the contrary, growth suppression of influenza A virus by RSV was observed when the coinfection began at the later stages of RSV infection. Suppression of the growth of RSV by influenza A infection was further demonstrated at the level of viral protein synthesis. An indirect immunofluorescence (IF) test revealed that a large proportion of infected cells synthesized both RSV and influenza A virus antigens. Scanning electron microscopic (SEM) examination demonstrated that influenza A and RSV virions possessing surface antigens specific for each virus were selectively released from dually infected cells. In the present study, we proved for the first time that the growth of RSV is blocked by competitive infection with influenza A virus in a susceptible cell population, competitive protein synthesis and selective budding of RSV and influenza viruses from the same infected cells.
机译:为了阐明呼吸道合胞(RSV)与流感病毒之间的流行病学干扰,研究了甲型流感(H1N1)病毒对RSV生长的影响。尽管RSV在MDCK细胞中生长,但与甲型流感病毒共感染导致后代RSV减少。生长干扰的程度取决于被RSV感染后(p.i.)感染甲型流感病毒的时间。实际上,在感染后的12小时内感染了甲型流感病毒。用RSV感染不会影响后一种病毒的生长。相反,当合并感染在RSV感染的后期开始时,观察到RSV抑制了甲型流感病毒的生长。在病毒蛋白合成水平上进一步证明了由甲型流感病毒感染抑制了RSV的生长。间接免疫荧光(IF)测试表明,大部分被感染的细胞都合成了RSV和A型流感病毒抗原。扫描电子显微镜(SEM)检查显示,具有双重抗原的A型流感病毒和RSV病毒粒子是从双重感染的细胞中选择性释放的,这些病毒具有每种病毒特有的表面抗原。在本研究中,我们首次证明RSV的生长受到易感细胞群中甲型流感病毒竞争性感染,竞争性蛋白质合成以及来自同一感染细胞的RSV和流感病毒的选择性萌芽的阻碍。

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