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.
Highlights
Applied at levels corresponding to those generated from the dielectric barrier discharge (DBD) plasma torch after 2 min (38.4 °C and 46.79 mJ/cm[2] UV, respectively)
feline calicivirus (FCV) has long been used as a surrogate for human norovirus in the evaluation of food preservation and disinfection processes[5,8,32,33,34,43]
Our results suggest that treatment with a DBD plasma torch is an effective means of inactivating FCV
Summary
Applied at levels corresponding to those generated from the DBD plasma torch after 2 min (38.4 °C and 46.79 mJ/cm[2] UV, respectively). Radical scavengers, including superoxide dismutase, dimethyl sulfoxide, and catalase, did not significantly affect viral titers; 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. Human norovirus is relatively resistant to heat and can survive temperatures as high as 60 °C (140 °F)[13] These thermal disinfection procedures can lead to nutritional loss and have an adverse effect on the food characteristics. There are no methods for the effective non-thermal inactivation of foodborne pathogens, especially human norovirus, that have completely satisfied all criteria, such as being non-toxic, non-irritant and economically viable
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