Research Institute, Taiko Pharmaceutical Co., Ltd, Suita, Osaka 564-0032, Japan.
J Gen Virol. 2012 Dec;93(Pt 12):2558-2563. doi: 10.1099/vir.0.044263-0. Epub 2012 Aug 29.
Airborne influenza virus infection of mice can be prevented by gaseous chlorine dioxide (ClO(2)). This study demonstrated that ClO(2) abolished the function of the haemagglutinin (HA) of influenza A virus (H1N1) in a concentration-, time- and temperature-dependent manner. The IC(50) during a 2 min reaction with ClO(2) at 25 °C was 13.7 µM, and the half-life time of HA with 100 µM ClO(2) at 25 °C was 19.5 s. Peptides generated from a tryptic digest of ClO(2)-treated virus were analysed by mass spectrometry. An HA fragment, (150)NLLWLTGK(157) was identified in which the tryptophan residue (W153) was 32 mass units greater than expected. The W153 residue of this peptide, which is derived from the central region of the receptor-binding site of HA, is highly conserved. It was shown that W153 was oxidized to N-formylkynurenine in ClO(2)-treated virus. It was concluded that the inactivation of influenza virus by ClO(2) is caused by oxidation of W153 in HA, thereby abolishing its receptor-binding ability.
气态二氧化氯（ClO2）可预防小鼠感染流感病毒。本研究表明，ClO2 以浓度、时间和温度依赖的方式使甲型流感病毒（H1N1）的血凝素（HA）失活。在 25°C 下与 ClO2 反应 2 分钟时的 IC50 为 13.7µM，而在 25°C 下用 100µM ClO2 处理时的 HA 半衰期为 19.5s。用质谱法分析了 ClO2 处理病毒的胰蛋白酶消化物产生的肽。鉴定到一个 HA 片段（150）NLLWLTGK（157），其中色氨酸残基（W153）比预期大 32 个质量单位。该肽的 W153 残基来自 HA 的受体结合位点的中心区域，高度保守。结果表明，ClO2 处理的病毒中 W153 被氧化为 N-甲酰犬尿氨酸。结论是，ClO2 使流感病毒失活是由于 HA 中的 W153 被氧化，从而使其丧失受体结合能力。
