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Ultrastructural Aspects of Photodynamic Inactivation of Highly Pathogenic Avian H5N8 Influenza Virus

机译:高致病性禽H5N8流感病毒光动力学失活的超微结构方面。

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摘要

Ultrastructural studies revealing morphological differences between intact and photodynamically inactivated virions can point to inactivation mechanisms and molecular targets. Using influenza as a model system, we show that photodynamic virus inactivation is possible without total virion destruction. Indeed, irradiation with a relatively low concentration of the photosensitizer (octacationic octakis(cholinyl) zinc phthalocyanine) inactivated viral particles (the virus titer was determined in Madin Darby Canine Kidney (MDCK) cells) but did not destroy them. Transmission electron microscopy (TEM) revealed that virion membranes kept structural integrity but lost their surface glycoproteins. Such structures are known as “bald” virions, which were first described as a result of protease treatment. At a higher photosensitizer concentration, the lipid membranes were also destroyed. Therefore, photodynamic inactivation of influenza virus initially results from surface protein removal, followed by complete virion destruction. This study suggests that photodynamic treatment can be used to manufacture “bald” virions for experimental purposes. Photodynamic inactivation is based on the production of reactive oxygen species which attack and destroy biomolecules. Thus, the results of this study can potentially apply to other enveloped viruses and sources of singlet oxygen.
机译:超微结构研究揭示了完整和光动力学灭活的病毒体之间的形态差异,可以指出灭活的机制和分子靶标。使用流感作为模型系统,我们表明光动力病毒灭活是可能的,而不会完全破坏病毒体。实际上,用相对较低浓度的光敏剂(八阳离子八(邻苯二甲酰基)锌酞菁)辐照灭活了病毒颗粒(病毒滴度在Madin Darby Canine Kidney(MDCK)细胞中测定),但并未破坏它们。透射电子显微镜(TEM)显示病毒体膜保持结构完整性,但丢失其表面糖蛋白。这样的结构被称为“秃头”病毒体,其首先由于蛋白酶处理而被描述。在较高的光敏剂浓度下,脂质膜也被破坏。因此,流感病毒的光动力失活最初是由表面蛋白去除引起的,随后是病毒体的完全破坏。这项研究表明,光动力处理可用于制造“秃头”病毒体以用于实验目的。光动力失活基于活性氧物质的产生,所述活性氧物质攻击并破坏生物分子。因此,这项研究的结果可能适用于其他包膜病毒和单线态氧来源。

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