紫外线诱导HIV-1感染性完全丧失的主要靶点:单链RNA包膜病毒的模型研究

IF 2 Q4 VIROLOGY
T. Koma, N. Doi, A. Suzuki, Kentaro Nagamatsu, Takeshi Yasui, K. Yasutomo, A. Adachi, T. Minamikawa, Masako Nomaguchi
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引用次数: 1

摘要

深紫外线(UV)可用于消毒微生物,包括细菌和病毒。尽管紫外线对基因组的损伤已被广泛接受,但紫外线对病毒蛋白(包括包膜成分)的活性和/或功能的不利影响却很少被记录在案。值得注意的是,观察到的紫外线对病毒的不利影响与病毒传染性的降低有关,但分析不足。在这项研究中,我们使用HIV-1作为单链RNA包膜病毒的模型,旨在阐明受紫外线影响的病毒粒子的哪个成分与病毒传染性的丧失显著相关。使用我们在三个波长(265、280和300nm)的紫外线照射设备,我们首先定量确定了降低传染性所需的每个波长的紫外线功率密度和照射周期。作为对照的热处理样品显著降低了病毒粒子相关逆转录酶(RT)活性和Gag-p24水平。三种波长的紫外线照射样品完全没有病毒感染性,显示出与未照射样品相似的p24水平。虽然病毒粒子相关的RT活性以波长和功率密度依赖的方式逐渐降低,但这种降低并不能解释紫外线导致病毒感染性的丧失。值得注意的是,病毒学分析显示,紫外线照射的病毒样本在三个波长下的进入效率与未照射的相当。重要的是,这一结果表明,即使暴露在致命水平的不同波长紫外线下的病毒粒子,仍保持其由宿主脂质双层和病毒蛋白组成的包膜的功能。与此形成鲜明对比的是,半定量RT-PCR显示的紫外线诱导的基因组损伤与病毒传染性的降低密切相关,表明它是紫外线灭活病毒的主要决定因素。研究发现,在所分析的区域中,损伤程度不同。这可能是由于通过PCR扩增的基因组区域中的核苷酸序列不同。我们的数据清楚地证明了紫外线灭活病毒的主要机制,并为改进基于紫外线的微生物消毒技术提供了信息。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Major target for UV-induced complete loss of HIV-1 infectivity: A model study of single-stranded RNA enveloped viruses
Deep ultraviolet light (UV) is useful for the disinfection of microorganisms, including bacteria and viruses. Although genome damage by UV has been widely accepted, the adverse effects of UV on the activity and/or function of viral proteins including the envelope components are poorly documented. Worthy of note, the observed unfavorable UV-effects for viruses are only insufficiently analyzed in association with the reduction in viral infectivity. In this study, we aimed to clarify which component of virions affected by UV significantly correlates with the loss of viral infectivity using HIV-1 as a model for single-stranded RNA enveloped viruses. Using our UV irradiation apparatus at three wavelengths (265, 280, and 300 nm), we first quantitatively determined the UV power density and irradiation period of each wavelength required for a reduction in infectivity. A heat-treated sample as a control drastically reduced the virion-associated reverse transcriptase (RT) activity and Gag-p24 level. The UV-irradiated samples at the three wavelengths, completely lacking viral infectivity, showed p24 levels similar to those without irradiation. While the virion-associated RT activity was gradually decreased in a wavelength and power density dependent manner, this reduction did not explain the loss of viral infectivity by UV. Remarkably, virological assays revealed that the entry efficiency of the UV-irradiated virus samples at the three wavelengths is comparable to those without irradiation. Importantly, this result shows that, even the virions exposed to UV of various wavelengths at the lethal level, still maintain the function of their envelope composed of a host lipid bilayer and viral proteins. In sharp contrast, UV-induced genome damage shown by semiquantitative RT-PCR correlated well with the reduction in viral infectivity, indicating that it is a major determinant for virus inactivation by UV. The degree of damage was found to be distinct among the regions analyzed. This was probably due to the different nucleotide sequences in those genomic regions amplified by PCR. Our data clearly demonstrate a principal mechanism for viral inactivation by UV and provide information contributing to the improvement of UV-based disinfection technology for microorganisms.
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