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不完全流感病毒:通过血细胞吸附细胞计数试验揭示的部分功能互补

Incomplete influenza virus: partial functional complementation as revealed by hemadsorbing cell count test.

作者信息

Kaverin N V, Kolomietz L I, Rudneva I A

出版信息

J Virol. 1980 May;34(2):506-11. doi: 10.1128/JVI.34.2.506-511.1980.

Abstract

In MDCK cells inoculated with an appropriate dilution of influenza virus, single hemadsorbing cells could be counted 8 h postinfection against a background of nonadsorbing cells. Standard virus preparation exhibited a linear relationship between the virus dilution and the number of hemadsorbing cells. With incomplete virus preparations obtained by passages of undiluted virus in chicken embryo, the dependence was nonlinear. A ts mutant (ts-29) of A/FPV/Weybridge (Hav1 Neq1) failed to convert MDCK cells into a hemadsorbing state at 42 degrees C. The ability of ts-29 to produce hemadsorbing cells could be rescued by incomplete wild-type virus. The capacity of incomplete virus for this partial functional complementation was inactivated by UV irradiation with one-hit kinetics. The size of the target was estimated to be 5.5 times smaller than that of the virus genome. The results suggest that at least some of the influenza virus genes in defective interfering particles are functional.

摘要

在接种适当稀释度流感病毒的MDCK细胞中,感染后8小时可在非吸附细胞背景下计数单个血细胞吸附细胞。标准病毒制剂在病毒稀释度与血细胞吸附细胞数量之间呈现线性关系。通过在鸡胚中传代未稀释病毒获得的不完全病毒制剂,这种相关性是非线性的。A/FPV/韦布里奇(Hav1 Neq1)的一个温度敏感突变体(ts-29)在42℃时无法将MDCK细胞转变为血细胞吸附状态。ts-29产生血细胞吸附细胞的能力可被不完全野生型病毒挽救。不完全病毒进行这种部分功能互补的能力通过单 hit 动力学的紫外线照射而失活。估计靶标的大小比病毒基因组小5.5倍。结果表明,缺陷干扰颗粒中至少一些流感病毒基因是有功能的。

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