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Key role of singlet oxygen and peroxynitrite in viral RNA damage during virucidal effect of plasma torch on feline calicivirus.

ABSTRACT: A dielectric barrier discharge (DBD) plasma torch has been used to evaluate the mechanism underlying inactivation of feline calicivirus (FCV) by plasma treatment. Plasma treatment of cell lysate infected with FCV F9 strain reduced the viral titer of the median tissue culture infectious dose (TCID50). The D value (treatment time required to lower the viral titer to 1/10) was 0.450?min, while the viral titer dropped below the detection limit within 2?min. FCV was not significantly inactivated by heat or UV applied at levels corresponding to those generated from the DBD plasma torch after 2?min (38.4?°C and 46.79 mJ/cm2 UV, respectively). However, TCID50 was reduced by 2.47?log after exposure to 4.62?mM ONOO-, corresponding to the concentration generated after 2?min of plasma treatment. Radical scavengers, including superoxide dismutase, dimethyl sulfoxide, and catalase, did not significantly affect viral titers; however, sodium azide, uric acid, and ascorbic acid, which are scavengers of 1O2 radicals, ONOO-, and peroxynitrous acid (ONOOH; produced from ONOO- under acidic conditions), respectively, significantly increased TCID50 and intact viral RNA. These findings suggest that ONOO- and 1O2 play an important role in FCV inactivation by attacking viral RNA during DBD plasma torch treatment.

SUBMITTER: Yamashiro R

PROVIDER: S-EPMC6298994 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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Project description:Human norovirus (NoV) is the leading cause of foodborne illnesses in the United States. Norovirus is shed in high numbers in the feces and vomitous of infected individuals. Contact surfaces contaminated with bodily fluids harboring infectious virus particles serve as vehicles for pathogen transmission. Environmental stability of NoV and its resistance to many conventional disinfectants necessitate effective inactivation strategies to control the spread of virus. We investigated the efficacy of two commercial disinfectants, hydrogen peroxide (7.5%) and a chlorine dioxide (0.2%)-surfactant-based product using a fogging delivery system against human NoV GI.6 and GII.4 Sydney strains as well as the cultivable surrogate, feline calicivirus (FCV) dried on stainless steel coupons. Log10 reductions in human NoV and FCV were calculated utilizing RNase RT-qPCR and infectivity (plaque) assay, respectively. An improved antiviral activity of hydrogen peroxide as a function of disinfectant formulation concentration in the atmosphere was observed against both GII.4 and FCV. At 12.4 ml/m3, hydrogen peroxide achieved a respective 2.5 ± 0.1 and 2.7 ± 0.3 log10 reduction in GI.6 and GII.4 NoV genome copies, and a 4.3 ± 0.1 log10 reduction in infectious FCV within 5 min. At the same disinfectant formulation concentration, chlorine dioxide-surfactant-based product resulted in a respective 1.7 ± 0.2, 0.6 ± 0.0, and 2.4 ± 0.2 log10 reduction in GI.6, GII.4, and FCV within 10 min; however, increasing the disinfectant formulation concentration to 15.9 ml/m3 negatively impacted its efficacy. Fogging uniformly delivered the disinfectants throughout the room, and effectively decontaminated viruses on hard-to-reach surfaces. Hydrogen peroxide delivered by fog showed promising virucidal activity against FCV by meeting the United States EPA 4-log10 reduction criteria for an anti-noroviral disinfectant; however, fogged chlorine dioxide-surfactant-based product did not achieve a 4-log10 inactivation. Future investigation aimed at optimizing decontamination practices is warranted.

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Key role of singlet oxygen and peroxynitrite in viral RNA damage during virucidal effect of plasma torch on feline calicivirus.

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